Unraveling the Gut–Skin Axis: The Role of Microbiota in Skin Health and Disease

Abstract

The complex interrelationship between the gut microbiota and the skin, commonly known as the “gut–skin axis” has become a crucial field of study for comprehending skin health and illness. Systemic immunity, inflammation, and metabolism are all modulated by this two-way communication mechanism, which ultimately affects skin homeostasis. Numerous dermatological disorders, such as rosacea, psoriasis, atopic dermatitis, and acne vulgaris, have been linked to dysbiosis in the gut microbiota. On the other hand, the composition of the gut microbiome may be impacted by skin disorders. Highlighting the important microbial metabolites and immunological processes involved in this interaction, this abstract examines the current understanding of the gut–skin axis. It also talks about the possible therapeutic benefits of using probiotics, synbiotics, and prebiotics to target the gut microbiota to treat and prevent skin conditions. Gaining insight into this intricate interaction opens up exciting possibilities for creating innovative, all-encompassing dermatological treatment strategies.

1. Introduction: A Comprehensive View on Skin Care

1.1. The Skin as a Barrier and Immune System

It is known that the largest organ in the body is represented by the skin, which covers its complete exterior [1]. The epidermis, the dermis, and the hypodermis serve as the three main layers of skin [2]. Together, these layers contribute to the skin’s main functions and defenses, such as sensation, thermoregulation, physical barrier, its immune system, and metabolism [2], by providing an effective barrier between the organism and the environment.

As the skin is the central sensory organ, it includes many different types of receptors which sense different stimuli, such as pain, temperature, pressure, and touch [3]. The principle of the thermoregulation system relies on different thermal signals being perceived by the superficial layer of the body and providing feedback afterwards, protecting the human body from extreme temperature fluctuations and dehydration [4,5]. Its physical barrier protects the body by preventing excessive water loss or absorption, blocking microorganisms, and shielding against mechanical injury, chemical exposure, and UV radiation [1].

The immune system of the skin is represented by an intricate link between skin cells and professional immune cells, which contribute to what we know as skin-associated lymphoid tissue (SALT) [6]. SALT includes different types of cells like keratinocytes, mast cells, B and T lymphocytes, and dendritic cells (DCs). Moreover, the skin is equipped with Toll-like receptors (TLRs) and NOD-like receptors (NLRs), where TLR2, TLR6, and NOD2 play key roles in recognizing and responding to common Staphylococcal and Streptococcal commensals and pathogens. TLRs 2, 3, 7, 8, and 9 are involved in detecting skin-tropic viruses, including herpesviruses, papillomaviruses, and poxviruses. Additionally, C-type lectin receptors, particularly Dectin-1, are crucial for recognizing and controlling fungal pathogens such as Candida albicans. Furthermore, keratinocytes detect bacterial signals and subsequently produce IL-1 family cytokines, which enhance key downstream processes, including wound healing and T cell activation [7]. Like aerodigestive epithelial cells, keratinocytes can express major histocompatibility complex (MHC) class II molecules in response to cytokines such as TNFα, IFNγ, or IL-22. While they are not known to prime naïve T cells, MHC class II expression by keratinocytes supports the expansion and activation of skin memory T cells. Inflammasome sensors like NLRP3 detect cellular damage and microbial invasion, triggering inflammasome assembly and activation of IL-1β. Dysregulated inflammasome activity contributes to autoinflammatory skin disorders and is implicated in common inflammatory conditions, including psoriasis, vitiligo, systemic lupus erythematosus, and atopic dermatitis [7]. Likewise, skin illnesses can be grouped into several main categories. Inflammatory conditions include eczema, acne vulgaris, and contact dermatitis. Despite being inflammatory skin disorders, eczema, acne vulgaris, and contact dermatitis vary greatly in their underlying causes, main symptoms, usual sites, and methods of treatment [8]. Epithelial tumors involve growth, like basal cell carcinoma, squamous cell carcinoma, and seborrheic keratosis. Pigment-related disorders, including albinism, moles, and melanoma, affect skin color and melanocyte function. Infectious skin diseases include bacterial infections like impetigo and cellulitis. Lastly, some metabolic diseases can show signs in the skin, since the epidermis is a tissue that quickly renews itself [3].

In addition to reflecting internal metabolic changes, the skin itself is metabolically active, taking part in processes involving glucose, protein, and lipid metabolism.

Glucose is the primary energy source for skin cells, with about 70% undergoing anaerobic glycolysis to produce lactic acid, which supports antimicrobial defense and systemic gluconeogenesis. A small portion enters the Tricarboxylic Acid (TCA) cycle, while the pentose phosphate pathway supports cell growth and repair. Glycogen serves as an energy reserve, especially during glucose shortage. Aging disrupts glucose metabolism, leading to glycation, advanced glycation end product (AGE) accumulation, and impaired skin structure and function [9]. The dangerous substances known as Advanced glycation end products (AGEs) are created when proteins and carbs interact. They cause wrinkles, sagging, and a lack of elasticity by harming important proteins like collagen and elastin, which accelerates the aging process of the skin [10]. Because they adversely affect multiple tissues by producing reactive oxygen species (ROS), aberrant proteins, or growth factors, changing the structure of the extracellular matrix (ECM), and secreting pro-inflammatory cytokines, AGEs are potentially harmful molecules that pose a threat to human health [11,12]. They damage the skin’s protective barrier, leading to dryness, and can impact skin cells, causing structural changes, hyperpigmentation, and the breakdown of collagen and elastin [13].

Protein metabolism is essential for skin integrity, with collagen being key to the dermal structure. Aging reduces collagen synthesis and increases degradation. Glutamine, a vital amino acid, supports energy production, cell growth, and wound healing. Reduced glutaminase activity with age may impair these processes and accelerate skin aging [9].

Lipids provide energy, structural support, and barrier protection in the skin. Fatty acids become critical energy sources during nutrient deficiency. Aging decreases lipid synthesis and increases lipid oxidation, weakening the skin barrier and contributing to dryness, thinning, and visible aging [9].

Moreover, the gut and skin host microbial populations. They are not accidental. They have an active effect on skin health. Also, they have an impact on skin conditions as well. When the gut microbiota is in equilibrium, skin immunity is enhanced. It promotes barrier function and lowers inflammation [14]. Different conditions can lead to dysbiosis when these microorganisms are out of balance. Many skin disorders are caused by dysbiosis. This covers common conditions, including eczema and acne. Chronic inflammatory conditions like psoriasis are also included [15]. It is encouraging to comprehend this interaction. New treatments may result from it. The gut microbiota will be the focus of these treatments. Enhancing skin health from the inside out is their aim [16].

Given the skin’s diverse physiological roles and its sensitivity to both internal and external factors, ongoing research is now directed toward the interplay between skin health and regulators such as the gut microbiota, which may influence cutaneous immunity, inflammation, and metabolic balance through the gut–skin axis.

1.2. The Gut Microbiota: A Key Player in Systemic Health Regulation

The gut microbiota represents an important component of the gastrointestinal tract, characterized as a vital organ that embodies a symbiotic relationship with its host, and it maintains different internal functions, like protection of the gastrointestinal barrier and metabolite digestion [17,18]. The human gastrointestinal tract hosts a vast and diverse community of over 100 trillion microorganisms [19]. The gut microbiota is primarily composed of six major phyla [20]. A diverse population of bacteria called the gut microbiota resides in the human digestive tract and is essential to controlling human general health. These microorganisms affect not only digestion but also our immune system, metabolism, mood, and brain function. The production of vitamins, defense against infections, and preservation of a healthy intestinal lining all depend on a diverse and balanced microbiota. Numerous illnesses are associated with disruptions to this delicate ecology, which are frequently brought on by poor food, stress, or antibiotics. This emphasizes the gut’s critical role in maintaining our overall health [21].

The metabolism of polyphenols, which contributes to their antioxidant and health-promoting properties, is also influenced by the gut flora. The amount consumed, the chemical makeup, and the bioavailability of polyphenols all affect their biological characteristics. Esters, glycosides, or polymers that are indigestible in their natural state are the most common forms of polyphenols found in food. Before these compounds may be absorbed, the intestinal bacteria must hydrolyze them. The outcome is the generation of several bacterial metabolites that enhance the polyphenols’ antioxidant potential and may have physiological effects [22,23].

Beyond digestion, the gut has its critical role, nutrient metabolism, with bacteria being the main contributors to ecosystem function due to their substantial genetic content. A key benefit of microbial metabolism is the conversion of both exogenous and endogenous substrates into nutrients that the host can utilize. Additionally, microbial metabolites can influence the immune system by affecting host cell physiology and gene expression [24].

Another critical role the gut microbiota has is synthesizing various essential vitamins, particularly vitamin K and several B-group vitamins such as biotin, cobalamin, folate, nicotinic acid, pantothenic acid, pyridoxine, riboflavin, and thiamine. Moreover, recent research in metagenomic sequencing has offered valuable insights into the specific pathways involved in vitamin biosynthesis by the gut microbiota [25,26].

Colonization resistance refers to the ability of the normal gut microbiota to prevent the invasion of external pathogens and the overgrowth of resident pathobionts. Evidence suggests that the indigenous gut microbes play a crucial role in protecting against pathogen colonization and intestinal infections. Although the exact mechanisms underlying colonization resistance are complex and not yet fully understood, they are recognized as essential to maintaining gut health [27].

The immune response, essential for infection control, consists of innate and adaptive systems. The innate immune system offers nonspecific defense through physical and chemical barriers and immune cells like macrophages and natural killer cells. The adaptive immune system provides antigen-specific protection via T cells, which mediate cellular immunity and regulate B cells. Moreover, B cells produce antibodies for humoral immunity. Together, they ensure comprehensive immune defense [28].

1.3. The Gut–Skin Axis’ Emergence

Both the skin and the gut function are active, intricate immunological and neuroendocrine organs frequently exposed to the external environment and harboring diverse microbiomes. The proper functioning of these two organs is essential for an organism to maintain homeostasis and ensure survival. Notably, the skin, as the body’s largest organ, acts as a primary defensive barrier against injuries and microbial invasion. Conversely, the gut hosts trillions of microbial communities, earning recognition as a “virtual organ” intrinsically linked to host health and longevity. The gut microbiome exerts both beneficial and detrimental influences on the normal physiology and homeostasis of both gut and skin tissues [16]. The gut and skin share many similar functions, especially concerning their immune, hormonal, and metabolic roles. The gut–skin axis is simply how closely the gut microbiota and the skin are connected. This idea was further developed into gut–skin–brain axis. This concept suggests that these three organs send complex signals to each other, influencing how the gut microbiota, our emotional states, and inflammation in the body and skin all interact [29]. A key recent study in mice strongly supports this idea. Erdman’s group showed that adding the probiotic Lactobacillus reuteri to the mice’s drinking water led to several beneficial changes in their skin. Mice given L. reuteri had thicker skin, more hair follicle growth, a more acidic skin pH, and produced more sebocytes [30].

It was also identified that modifications in the microbiome affect immune responses and skin, leading to urticaria, often accompanied by gastrointestinal symptoms, conditions such as irritable bowel syndrome, and inflammatory bowel disease, which can also manifest as dry skin and itching [31]. Accordingly, this connection between digestive issues with skin conditions was supported by dermatologists John H. Stokes and Donald M. Pillsbury over 70 years ago, when a theory suggesting a gastrointestinal link among emotional states and skin conditions such as acne was introduced [32] (Figure 1).

The interplay between the gut microbiome and the skin is driven by several key mechanisms. One significant pathway is immunomodulation, where the gut microbiome influences the body’s overall immune response, directly affecting skin inflammation and immune function. Hormonal pathways are also crucial; hormones produced in response to gut microbial activity can impact skin physiology. Additionally, gut bacteria generate various metabolites, such as short-chain fatty acids (SCFAs). These SCFAs can enter the bloodstream and influence skin cells, helping to regulate the skin barrier and inflammatory processes. Interestingly, emerging research now suggests this axis is bidirectional, meaning the condition of the skin might also influence the gut microbiome [33].

However, recent advancements in metagenomics and metabolomics provide modern scientific validation to the gut–skin axis with different multi-omics approaches, including the following: studying of the sequences and functions of all genetic information extracted from a specific site with metagenomics and the analysis of small molecules, known as metabolites, intermediates, products of cell metabolism in cells, tissues, or organisms with metabolomics [33] (Figure 1).

Both animal and human experiments are frequently used in the research on this subject. The processes by which gut microbes affect skin health are studied in animals. For instance, some of the research cited in the search results examines how probiotics, such as Lactobacillus reuteri, affect mice’s skin. These investigations have shown fundamental biological mechanisms and established causation. Changes in the commensal skin microbiota may facilitate the development of chronic wounds. Probiotics may prevent and treat non-healing wounds, according to recent studies conducted in animal models. In comparison to controls that received silver sulfadiazine treatment, kefir extracts in topical gels have improved the epithelialization and collagen production in burn injuries in rats [34]. The immunomodulatory potential of probiotics in skin tissues was demonstrated when oral probiotics were given to UV-injured mice, which changed the number of immune cells in the skin as well as the levels of IL-10 [35]. In comparison to controls, mice’s healing processes were accelerated when lactic acid bacteria were added to their drinking water. Furthermore, by promoting oxytocin, which in turn stimulated the CD4 + Foxp3 + CD25 + Treg cells that transmit the wound healing potential, the probiotic strain Lactobacillus reuteri enhanced wound healing [36]. These findings lend credence to the idea that Tregs can influence the immune system outside of the gut.

A crucial element is also human trials. The “human trials” mentioned in the research results highlight the promise of treatments that target the gut microbiota, such as probiotics and prebiotics, to treat diseases like atopic dermatitis and psoriasis. These studies investigate whether altering the gut microbiota can benefit actual people’s skin health. Probiotics and postbiotics are examples of emerging medicines that seek to restore microbial diversity, whereas phage therapy targets harmful bacteria like Staphylococcus aureus specifically without affecting beneficial flora. Clinical trials have shown that patients receiving these microbiota-targeted therapies have improved quality-of-life indicators and have seen significant decreases in inflammatory lesions [37]. The evidence currently available on the reciprocal interactions between skin microbiota and metabolic diseases is summarized in this review, along with potential treatment applications and future directions. Precision techniques in dermatology are opening the door to better patient outcomes by tackling microbiota-mediated pathways and systemic metabolic dysregulation [37].

Thus, the hypothesis was defined as follows: gut dysbiosis contributes to systemic inflammation and alters immune responses, thereby influencing skin homeostasis and disease susceptibility.

1.4. Scope of the Review

This review critically examines the mechanistic pathways and therapeutic potential of targeting the gut microbiota in dermatological diseases. It highlights how gut microbes influence skin physiology through immune, metabolic, and neuroendocrine pathways and how gut dysbiosis can contribute to the pathogenesis of common dermatological conditions such as atopic dermatitis, acne, psoriasis, and rosacea. This review explicitly examines the primary mechanisms underlying this link, such as the following:

The anti-inflammatory properties of microbial metabolites, like short-chain fatty acids (SCFAs), aid in maintaining the integrity of the intestinal barrier. A key factor in psoriasis inflammation is the modulation of immune pathways, specifically the Th17/IL-17 axis. Neuroendocrine communication between the gut and brain can impact stress and inflammation of the skin. Lastly, the creation of vital vitamins and the function of other microbial metabolites also affect skin health. This article also investigates emerging microbiome-targeted therapies, including probiotics, prebiotics, postbiotics, and dietary interventions, and discusses future directions for research and clinical application in dermatology.

This manuscript critically acknowledges important challenges like individual response variability, regulatory concerns, and the current limitations of clinical data while thoroughly examining the therapeutic potential of targeting the gut microbiota in skin health. It does this by integrating multidisciplinary insights and discussing recent clinical trials and novel microbial targets.

A thorough and organized literature search across important scientific databases was used to perform this review. A methodical strategy was used to identify pertinent peer-reviewed publications, utilizing medical subject headings (MeSH) terms and targeted keywords. The selection process was governed by stringent inclusion and exclusion criteria, prioritizing research on the gut–skin axis, its processes, and targeted treatments. Original research, reviews, and meta-analyses published in English were among the chosen articles. Following that, information about gut microbiota activities, skin physiology, and the complex relationships between the gut and skin was taken from these sources and combined. The goal of the project was to conduct a narrative synthesis of existing information, including the role gut dysbiosis plays in dermatological diseases. Research on immunological, metabolic, and neuroendocrine pathways as well as newly developed microbiome-targeted therapies was highlighted. A comprehensive and fact-based understanding of the area is guaranteed by this exacting methodology.

2. The Gut Microbiome: Composition, Function, and Dysbiosis

2.1. Normal Gut Microbiota Composition

The human gut microbiota is predominantly characterized by two dominant phyla: Firmicutes (Gram positives) and Bacteroidetes (Gram-negative anaerobes) [38]. Together, these phyla typically constitute approximately 90% of the total gut microbial community [19], with Actinobacteria, Proteobacteria, Fusobacteria, and Verrucomicrobia. The key genera of Firmicutes are defined by Lactobacillus, Bacillus, Clostridium, Enterococcus, and Ruminicoccus [39], while Bacteroidetes are primarily represented by Bacteroides and Prevotella [19]. Actinobacteria consists of Bifidobacteria, Atopobium, and Collinsella, the Proteobacteria of Enterobacteriaceae [38].

All these microbial communities contribute to stability and diversity, which marks the importance of a rich and stable community. Balance is expressed by local stability, which refers to the system’s local management near the equilibrium in addition to small disruptions and external stability, which marks the capacity of the community to resist the intrusion of new species [40]. The gut microbiota exhibits a high amount of resilience, which is the state of an ecosystem before external perturbations, enabling the host to maintain core microbial species over extended periods. The remarkable long-term stability of the gut microbiota in healthy adults is not an immutable state but rather a dynamic equilibrium that can be significantly altered by a variety of factors, including early life exposure, genetics, diet, and medications [41].

Also, gut microbiota composition shows significant correlations with personality traits, often aligning with observations in human psychiatric conditions and animal models. For instance, Akkermansia, Lactococcus, and Oscillospira genera are more abundant in individuals with higher sociability, consistent with findings in autism and mouse studies; notably, Akkermansia and Oscillospira are associated with positive health indicators. Conversely, Desulfovibrio and Sutterella are more prevalent in less sociable individuals, mirroring their elevated levels in autism and even hypothesized roles in its pathophysiology. Furthermore, neurotic tendencies negatively predict the abundance of Streptococcus and Corynebacterium, suggesting lower levels of these genera in more neurotic individuals. While this aligns with Corynebacterium reductions in stress-induced depression models, the relationship with Streptococcus in depression has shown contrasting findings. Overall, these relationships suggest a complex interplay between specific gut microbial genera and host personality dimensions, particularly sociability and neuroticism [42].

The mode of delivery plays a crucial role in shaping the initial gut microbiota, with vaginally and cesarean-delivered neonates exhibiting distinct microbial compositions. Culture-based analyses revealed that staphylococci predominated in meconium, while enterococci and certain Gram-negative bacteria (e.g., Escherichia coli, Klebsiella pneumoniae, or Serratia marcescens) were more abundant in fecal samples. Complementary 16S rRNA gene-based microarrays further showed a high prevalence of bacteria related to Streptococcus mitis and Lactobacillus plantarum in meconium, contrasting with the predominance of taxa related to E. coli, Enterococcus, and K. pneumoniae in infant feces [43]. Vaginal birth facilitates early colonization by maternal microbes, leading to higher bacterial counts in the infant gut compared to those delivered via cesarean section [44]. Cesarean-section delivery significantly influenced the abundance of only one genus, Flavonifractor, leading to its higher prevalence in individuals born via this method [42].

Individuals within the same family often exhibit more similar microbial profiles than unrelated individuals. These familial similarities are largely attributed to shared environmental factors, particularly diet, which is a major determinant of microbiome composition. However, the greater genetic similarity among relatives also suggests a potential role for host genetics in shaping the microbiota [45]. Other studies have revealed that host genetics significantly influence gut microbiome composition. Phylogenetically related species tend to have more similar microbiotas, even when their diets and lifestyles differ. For instance, human gut microbiomes are more alike across continents than they are compared to those of other mammals. This idea is also sustained by a study which, using two different comparison methods, has shown that even though people’s gut bacteria differ across continents and ages, surprisingly, the human gut bacteria are more alike among themselves than they are to those of any other mammal [46]. Similar patterns are seen in great apes, where gut microbiome phylogenies mirror mitochondrial DNA relationships. However, diet seemed more important than family tree in shaping their gut bacteria and then humans’ gut bacteria grouped with other omnivores. Even with our modern, varied diets, our gut bacteria are not drastically different from other omnivorous primates, but more study is needed [46]. Additionally, experiments show that germ-free mice colonized with human microbes revert to a mouse-specific microbiota, highlighting host-driven selection. Within species, genetic variation also plays a role, as shown by greater microbiome similarity in monozygotic compared to dizygotic twins [47].

Furthermore, the microbiota’s makeup is greatly impacted by dietary patterns, which can be modified by nationality, religion, and the type of cuisine consumed. This is why the diversity in gut microbiome composition seen throughout populations is a powerful illustration of how dietary and cultural behaviors can affect microbial ecosystems. In healthy Europeans, including individuals of Slavic origin, microbiota is dominated by the phyla Firmicutes, Bacteroidota, Actinobacteria, Proteobacteria, Fusobacteria, and Verrucomicrobia. Among African populations, Bacteroides and Prevotella are predominant. Asian individuals typically exhibit a highly diverse microbiota enriched in genera such as Prevotella, Bacteroides, Lactobacillus, Faecalibacterium, Ruminococcus, Subdoligranulum, Coprococcus, Collinsella, Megasphaera, Bifidobacterium, and Phascolarctobacterium. Religious dietary patterns also appear to shape microbiome profiles, with Prevotella-dominated enterotypes common among Buddhists and Muslims, and Bacteroides-dominated enterotypes more prevalent among Christians [48].

The gut–skin axis refers to the close association between the dysbiosis of the gut microbiota and the dysbiosis of the skin microbiome. A key idea in contemporary immunology and dermatology is this link. An increasing amount of research demonstrates that many inflammatory skin disorders are associated with alterations in the gut microbiota beyond being local skin issues [49].

Compared to healthy people, psoriasis patients have a markedly different skin microbiome in both their lesional (affected) and non-lesional (unaffected) skin. One important discovery is that psoriatic patients’ skin microbiomes have significantly lower alpha diversity or the number of distinct bacterial species in a single sample. In the actual psoriatic lesions, this reduction is significantly more noticeable [50].

Beneficial or commensal bacteria such as Lactobacilli, Burkholderia, and Cutibacterium acnes are becoming less common [50]. On the other hand, potentially harmful bacteria like Neisseria species, Finegoldia species, Corynebacterium kroppenstedii, and Corynebacterium simulans are becoming more prevalent. Additionally, several investigations have found that psoriatic skin has a higher concentration of Streptococcus and Staphylococcus species [51].

Another obvious example is atopic dermatitis. The gut microbiome of AD patients frequently has less diversity and more of some bacteria, like Escherichia coli and Clostridium difficile. Staphylococcus aureus overgrowth on the skin is well-documented and contributes to inflammation and the breakdown of the skin barrier. Acne is another condition where the relationship is seen. Acne patients frequently have gut dysbiosis, which is typified by a change in the skin’s Cutibacterium acnes strain profile and a decline in good bacteria [52].

From an animal and plant-based diet, distinct effects can be observed based on dietary patterns. Animal-based diets, particularly those high in fat and protein, are associated with increased levels of Bacteroides, Firmicutes, and Proteobacteria, while beneficial bacteria such as Lactobacillus and Roseburia tend to decrease. These changes are linked to reduced microbial diversity and increased production of pro-inflammatory molecules such as lipopolysaccharides (LPSs) and trimethylamine-N-oxide (TMAO), contributing to chronic low-grade inflammation, metabolic endotoxemia, and insulin resistance. In contrast, plant-based diets, rich in fiber and resistant starches, promote the growth of Prevotella, Bacteroides, and short-chain fatty acid (SCFA)-producing bacteria. These diets are associated with increased microbial diversity, enhanced SCFA production, improved gut barrier function, and reduced inflammation [53].

Also, medications play a crucial role in gut microbiota composition. Antibiotics have a dual effect by eradicating both pathogenic and beneficial microorganisms, often leading to gut microbiota disruption or dysbiosis. This imbalance impairs essential microbial functions, including competitive exclusion, a key mechanism through which commensal microbiota prevents the colonization and overgrowth of opportunistic pathogens [54].

2.2. Functional Roles of the Gut Microbiome

Some of the most important functional roles of the gut microbiome are in human metabolism, a key factor for different microbial pathways such as the fermentation of dietary fiber into SCFAs, bile acid assimilation, and xenobiotic detoxification [25].

As previously mentioned, the fermentation of dietary fibers results in SCFAs, and the three most commonly detected in feces are acetate, propionate, and butyrate [25]. They play an important role in maintaining the barrier function of the intestinal tract, are anti-inflammatory [55], have a specific mechanism in inflammatory bowel diseases [56], but also have an immune regulation function [55]. Moreover, SCFAs could potentially have an anti-cancer effect because of butyrate’s capacity to induce apoptosis in colon cancer cells [25].

Regarding bile acids, one of their fundamental functions is to promote the emulsification of dietary fats and to assist intestinal absorption [57]. They also appear to be a major regulator of the gut microbiota, as the bile acid pool size and composition have been directly linked to cirrhosis [58].

Furthermore, xenobiotic detoxification is made chemically by the gut microbiome, through the intestinal tract or re-entering the gut by enterohepatic circulation.

In addition, the gut microbiome can reduce xenobiotic absorption in the small intestine by upregulating cell-to-cell adhesion proteins, reinforcing the integrity of the mucosal barrier, and directly binding to chemical compounds. In addition, microbial communities influence host gene expression, including genes encoding cytochrome P450 enzymes, multidrug resistance transporters, and their associated transcriptional regulators. While the microbiome modulates host responses and the pharmacokinetics of xenobiotics, xenobiotics in turn can alter microbial viability and metabolic activity [59].

However, the gut microbiota significantly influences host immunity and health through various intricate mechanisms. This includes the modulation of immune responses and the promotion of intestinal homeostasis by probiotics, prebiotics, and postbiotics, which are shown to regulate cytokine production and maintain gut barrier integrity [60]. Furthermore, the interaction between the gut microbiota and the immune system involves the critical role of toll-like receptors (TLRs) on T cells. These interactions are fundamental in modulating T-cell differentiation, guiding adaptive immune responses, and ensuring intestinal tolerance or pathogen defense, thereby underscoring the deep mutual regulation between the microbiota and the host’s immune system [61].

Ultimately, the intestinal barrier’s structural and functional integrity relies heavily on tight junction (TJ) proteins and the mucus layer, both of which are strongly influenced by the gut microbiota. Commensal bacteria and their metabolites, particularly short-chain fatty acids such as butyrate, have been shown to enhance the expression of TJ proteins like claudins and occludin, thereby reinforcing epithelial cohesion and reducing paracellular permeability [62]. Additionally, microbial modulation of mucin production helps maintain the mucus barrier, with certain species like Akkermansia muciniphila promoting mucin turnover that supports barrier function without compromising its integrity [63]. Disruption in microbial communities can impair TJ integrity and mucus dynamics, contributing to increased gut permeability and susceptibility to inflammation [64].

2.3. Gut Dysbiosis: Definition and Consequences

Dysbiosis is a complex disruption of the gut microbiota’s homeostatic balance. This state involves a shift from a beneficial microbial community to one that is functionally compromised and associated with disease [65]. Such imbalances can manifest through alterations in the gut flora’s taxonomic composition, changes in their collective metabolic activities, or modifications to their spatial organization within the gastrointestinal lumen. Ultimately, dysbiosis creates an internal environment that can actively promote the development and progression of various pathological conditions [66].

The intricate ecosystem of the gut microbiota, vital for maintaining host physiological processes, is highly sensitive to a variety of internal and external influences. Identifying the principal causes of gut dysbiosis is fundamental to understanding its role in disease pathogenesis and to developing targeted interventions for its prevention and reversal.

The main causes are represented by antibiotics, psychological and physical stress, and dietary factors [67]. These factors can lead to dysbiosis-related diseases, such as type 1 diabetes, allergies, necrotizing enterocolitis, and obesity [68].

Thus, due to different shifts in the gut, dysbiosis can have consequences by harming the host, disrupting the gut barrier, and unbalancing immune and metabolic systems. Microbial factors, like acetaldehyde or mucolytic activity, compromise intestinal integrity. Simultaneously, microbial molecules modulate immunity by inflammasome, TLR, and NLR signaling, favoring inflammation. Metabolically, dysbiosis alters glucose and lipid metabolism through changes in bile acids and SCFAs, among others [69].

3. Therapeutic Strategies Targeting the Gut Microbiome for Skin Health

3.1. Dietary Interventions

Fiber-Rich Diets: Promote SCFA production and overall gut health.

The human gut microbiota ferments dietary fiber, resulting in the production of short-chain fatty acids and other probiotic metabolites. Due to a significant decline in dietary fiber consumption over the past few centuries, gut microbiota has undergone harmful changes. These shifts in dietary fiber intake have played a role in global obesity, type 2 diabetes, skin problems, and other metabolic disease epidemics [70]. Over the past few decades, there has been much discussion on what constitutes dietary fiber. Oligosaccharides, a class of resistant carbohydrates with three to nine monomeric units (MU), were the subject of the dispute. “Carbohydrate polymers with ten or more MUs, which are resistant to hydrolysis by endogenous enzymes and absorption in the small intestine of humans” are classified as dietary fiber in the officially published Guidelines on Nutrition Labeling (modified in 2009) [71]. Subsequent research, however, found that indigestible oligosaccharides and polysaccharides that contain similar monosaccharides undergo homogeneous fermentation and physiological activities, supporting the idea that oligosaccharides are a type of dietary fiber (DF) in their official guidelines or standards [72,73,74].

DFs can affect the gut microbial ecosystem by changing its composition in terms of taxonomic presence/absence, relative abundance, and metabolism according to their characteristics (such as resistance to digestion by host enzymes and fermentability by intestinal bacteria). According to reports, distinct microorganisms have varying capacities for metabolizing DFs, resulting in the generation of distinct end products [75]. A remarkable variety of carbohydrate-active enzymes (CAZymes), which are encoded differently by different gut bacteria, are needed for the metabolization of DFs, which have diverse physicochemical characteristics [76,77]. Therefore, it is structure-dependent and may involve many metabolic pathways for the gut bacteria to ferment DFs [76]. Short-chain fatty acids (SCFAs), including acetate, propionate, and butyrate, as well as gases like H₂ and CO₂, are the main byproducts of the gut fermentative action on DFs [78]. Anaerobic gut bacteria create SCFAs that are beneficial to human health, including immunological homeostasis maintenance, metabolic activities, glucose homeostasis, intestinal barrier integrity, and hunger management [78] (Figure 2).

According to their functional activities, these metabolites appear to be beneficial in the prevention and treatment of several diseases [79] (Figure 2). Dysbiotic settings associated with disease tend to have lower levels of these metabolites, as well as those produced by gut microbes [80]. As a result, DFs and the related host health are actively linked by the gut microbiota. SCFA levels in plasma and serum range from 50 to 100 μmol/L for acetate and from 0.5 to 10 μmol/L for propionate and butyrate, which are significantly lower than those in the colon lumen [81].

Dietary fiber has been linked to beneficial effects on inflammation beyond the gastrointestinal tract. The pro-inflammatory chemokine monocyte chemoattractant protein-1 (MCP-1/CCL2) and pro-inflammatory cytokines interleukin-18 and interleukin-33 were shown to be secreted less frequently in rheumatoid arthritis (RA) patients who received a high-fiber dietary intervention [82]. By encouraging T regulatory cells (Tregs) and inhibiting T follicular helper (Tfh) and Th17 cells, butyrate administration demonstrated anti-inflammatory effects in mice with collagen-induced arthritis (CIA) [83]. A high-fiber diet high in resistant starch was found to significantly reduce bone damage and CIA. It also changed the composition of gut microbes and increased the amount of circulating propionate, which is another byproduct of fiber fermentation in vivo, according to another study [84].

It is essential to remember that different people experience different outcomes while consuming the same amount of dietary fiber. Because everyone’s gut microbiota is different, so is how dietary fiber is metabolized, which can have a range of effects [85]. Understanding diet–microbiota–host interactions now requires taking into account the inter-individual heterogeneity in SCFA production. Recent research highlights that individual differences in gut microbiota composition, host genetics, and long-term dietary patterns greatly affect SCFA production capacity, even if dietary fiber consumption is a major predictor of SCFA yield [86]. Prevotella-dominated individuals are better at digesting fibers rich in arabinoxylan into propionate, whereas Ruminococcus or Faecalibacterium prausnitzii-dominated individuals preferentially create butyrate. The amount and ratio of acetate, propionate, and butyrate generated are influenced by the relative abundances of Firmicutes and Bacteroidetes, especially those that break down fiber [25].

Furthermore, microbial colonization patterns and fermentation efficiency may be impacted by host genetic variations, such as those in genes controlling mucin secretion or immune response (Figure 2). This heterogeneity is also influenced by environmental factors such as the use of antibiotics, physical activity, and regular fiber consumption [25]. Generally speaking, there are two primary categories of dietary fiber according to their solubility. According to Khorsaniha et al. [87], insoluble dietary fiber (IDF) does not dissolve in water, whereas soluble dietary fiber (SDF) does. Psyllium, glucomannan, mucilage, carrageenan, arabinoxylan, arabinogalactan, guar gum, alginate, inulin, beta-glucan, fructooligosaccharides (FOSs), galactooligosaccharides (GOSs), pectin, and beta-glucan are some of the types of SDFs [88]. Because of its physicochemical characteristics, including its water-binding ability, fermentability, and viscosity, SDF has different effects on the gut environment [89]. SDF is known to improve microbial diversity and balance and provides the gut microbiota with energy. For example, GOS enhances the growth of anti-inflammatory bacteria, whereas FOS encourages the growth of Bifidobacteria and Lactobacilli.

In conclusion, dietary fiber is crucial for human health, primarily through its fermentation by gut microbes into short-chain fatty acids (SCFAs) (Figure 2). A decline in fiber intake negatively impacts the gut microbiota, contributing to an increase in metabolic diseases. DFs, including oligosaccharides, modify the gut ecosystem and produce SCFAs vital for immune, metabolic, and intestinal health. These benefits extend systemically, reducing inflammation throughout the body. However, individual responses to fiber vary due to unique gut microbiomes, genetics, and lifestyle. Both soluble (SDF) and insoluble (IDF) fibers contribute to microbial diversity and beneficial metabolic activities. In essence, dietary fiber is fundamental for a healthy gut and overall well-being, highlighting the critical link between diet, microbiota, and host health.

Prebiotic-Rich Foods: Fructans and galactooligosaccharides (GOSs)—nourishing beneficial gut bacteria.

The term “prebiotic” refers to a non-digestible food element that enhances host health by selectively promoting the growth and/or activity of one or a small number of bacteria in the colon [90]. Prebiotics are defined as follows: (1) they must be resistant to the stomach’s acidic pH; mammalian enzymes must not hydrolyze them and they cannot be absorbed in the gastrointestinal tract; (2) they must be fermentable by intestinal microbiota; and (3) they must be able to selectively stimulate the growth and/or activity of the intestinal bacteria, improving the host’s health in the process [91]. Prebiotics come in several varieties. Most of them are oligosaccharide carbohydrates (OSCs), which are a subset of carbohydrate families. Although the majority of the pertinent publications focus on OSCs, there is some indication that prebiotics are more than just carbs [92]. In addition to other fibers and certain non-carbohydrate substances, common prebiotics include non-digestible fermentable carbohydrates such as galactooligosaccharides (GOSs), resistant starches, and fructans (e.g., inulin and FOS) [93]. Prebiotics promote a balanced skin microbiome, improve skin barrier function, lower inflammation, increase hydration, and create a more resilient, glowing complexion by feeding the good bacteria (probiotics) that live on and in the body. This can occur through the “gut–skin axis,” in which oral prebiotics have a beneficial effect on gut health, which in turn affects skin health, or by the topical application of prebiotic skincare products [94]. Although the preventive properties and functions of topical probiotics help preserve the skin’s homeostasis, their drawbacks and limitations can lead to inflammatory skin diseases that are challenging to treat fully with topical probiotics. The effectiveness and side effects of internal probiotic formulations for treating wound healing, psoriasis, acne, atopic dermatitis, and various other skin conditions are being investigated in several clinical trials [94].

Anti-Inflammatory Diets: Mediterranean diet principles, avoidance of highly processed foods, excessive sugar, and unhealthy fats.

Healthy skin is intrinsically linked to an anti-inflammatory diet because the Mediterranean diet is naturally anti-inflammatory, as it is rich in fruits, vegetables, whole grains, legumes, nuts, seeds, olive oil, and lean proteins such as fish [95]. These foods are rich in polyphenols, omega-3 fatty acids, and antioxidants, all of which actively fight inflammation and oxidative stress in the body. A diet that helps reduce systemic inflammation can lead to healthier skin by lowering inflammation and redness. This approach directly addresses and helps alleviate symptoms of various skin conditions such as acne, rosacea, eczema, and psoriasis [95]. In this way, diet is presented as a therapeutic tool for managing existing skin pathologies. Dietary factors that affect hormonal and metabolic pathways, particularly insulin and insulin-like growth factor 1 (IGF-1), are the main causes of acne. Blood glucose concentrations rise quickly in diets strong in high-GI carbs (such as white bread and processed sweets) [96]. This causes insulin levels to rise, which raises IGF-1 levels. Because it enhances androgen activity, increases sebocyte proliferation, and increases sebum production, elevated IGF-1 plays a crucial role in the pathophysiology of acne. On the other hand, some studies have demonstrated that a low-GI diet can lessen acne lesions by reducing these hormonal cascades [97]. The exact mechanisms by which high-GI foods contribute are also involved in the insulinotropic impact of different milk components, especially whey protein, which raises IGF-1 levels on its own. Even though this link is widely known, research is still ongoing to determine the actual ingredients in dairy and their consequences [98]. In contrast to acne, rosacea is typified by neurogenic inflammation and vascular hyperreactivity. Vasodilation is intimately linked to dietary stimuli, which are typically more immediate.

Rosacea flare-ups are frequently triggered by foods and drinks that dilate blood vessels, which results in the characteristic flushing and redness. These include hot beverages, alcohol (particularly red wine), and spicy foods that include capsaicin. These elements can all activate transient receptor potential (TRP) channels, which can cause a neurogenic inflammatory response [99]. Histamine-rich meals, including processed meats, aged cheeses, and some fermented foods, can potentially cause vasodilation and worsen symptoms in those who are vulnerable [99]. There has been increasing evidence linking rosacea to dysbiosis, or a change in the gut flora. Anti-inflammatory diets and the addition of probiotics and prebiotics may have some advantages by enhancing gut health and, consequently, reducing skin inflammation, while research is still being conducted [100].

The integrity of the skin barrier and immunological responses are the two factors most strongly associated with food and eczema. Food allergies affect a significant percentage of atopic dermatitis patients, particularly children. Allergens (such as cow’s milk, eggs, peanuts, and wheat) can cause a systemic immune response, which releases inflammatory mediators that exacerbate the symptoms of eczema. In order to prevent nutritional shortages, elimination diets are only advised under medical supervision following a verified allergy [101]. The balance of omega-3 and omega-6 fatty acids partially regulates the defective skin barrier, a significant mechanism in eczema. Inflammation may worsen if there is a high proportion of pro-inflammatory omega-6 to anti-inflammatory omega-3 fatty acids [102]. Although there is conflicting evidence about the effectiveness of gamma-linolenic acid (GLA), an omega-6 fatty acid included in evening primrose oil that has anti-inflammatory qualities, several studies have looked into the possible advantages of supplementing with it [103].

Psoriasis is a long-term autoimmune condition that is caused by a complex inflammatory process. Systemic inflammation and metabolic health are the main ways that diet affects this illness [104]. It has been demonstrated that psoriasis is made worse by a Western diet that is heavy in red meat, processed carbohydrates, saturated fats, and alcohol. These foods can trigger inflammatory pathways that are essential to the pathophysiology of psoriasis, such as the NLRP3 inflammasome and the IL-23/IL-17 axis [105]. Diets high in anti-inflammatory ingredients, like the Mediterranean diet, on the other hand, may be advantageous. These diets focus on foods that help lower systemic inflammation, such as fruits, vegetables, seafood (high in omega-3 fatty acids), whole grains, and healthy oils [106].

Dietary antioxidants prevent wrinkles and preserve skin suppleness by scavenging free radicals that break down collagen and elastin [107]. Nuts, seeds, and vegetable oils, which are key components of the Mediterranean diet, are excellent sources of alpha-tocopherol (Vitamin E). Significant amounts of this vitamin are also found in leafy green vegetables and fortified cereals. This protective mechanism helps to preserve skin suppleness and prevent the formation of wrinkles. [108]. The Vitamin E in the human body directly influences the health of tissues, including your skin. Sebum, the skin’s natural oily substance, is rich in Vitamin E and continuously releases it into the outer layers of the epidermis, thereby offering protection to the skin [26].

Healthy fats, especially those found in fatty fish and olive oil, help to create a robust lipid barrier that shields the skin from environmental aggressors and keeps moisture in [109].

Consuming a Western diet, such as large amounts of sugar, inadequate fats, and overly processed foods, can cause widespread inflammation, which can seriously damage your skin. Unhealthy fats, artificial chemicals, and refined carbohydrates are frequently found in highly processed foods [110]. Rapid blood glucose surges and systemic inflammation brought on by these substances accelerate aging, worsen breakouts, and leave skin looking lifeless.

A condition known as glycation is triggered by an excess of glucose, which binds to skin proteins such as collagen and elastin, causing them to become brittle and rigid. This causes sagging and wrinkles. Additionally, glucose directly contributes to inflammation and can exacerbate acne by increasing oil production [111]. Lastly, inflammatory indicators in the body can be elevated by harmful fats, including trans and saturated fats, which are commonly found in processed and fried foods [112].

3.2. Probiotics

Live microorganisms that, when administered in adequate amounts, confer a health benefit on the host. It is essential to understand the concept of strain specificity when considering probiotics for skin health. This suggests that specific strains of probiotics, rather than the overall species or genus, are often associated with their beneficial effects. Different strains can have distinct mechanisms of action and, therefore, exert different effects on the host’s health, including the skin [113].

For instance, although many Lactobacillus species are well-known for their general probiotic advantages, several studies demonstrate that Lactobacillus rhamnosus GG (LGG) is especially effective for treating diseases like atopic dermatitis (DA). Research has shown that when administered in sufficient quantities, LGG can help individuals with DA achieve better skin health outcomes [114]. According to some theories, this is due to its unique immunomodulatory qualities and capacity to affect the gut–skin axis, which in turn helps restore the skin barrier and reduce inflammation in afflicted individuals [16].

Therefore, rather than merely looking for a general probiotic designation, it is crucial to find products or advice that specifically name the strain that has been clinically established to provide the required benefit when looking for probiotic support for skin health [115].

Modes of Action Probiotics employ a variety of complex mechanisms, often in concert, to produce their positive effects on skin health. These methods of action consist of immune modulation. When applied topically, probiotics can directly affect the skin’s immune cells. When consumed, they can also indirectly affect the gut–skin axis. By lowering pro-inflammatory cytokines and increasing anti-inflammatory ones, they often help balance the immune response [94]. This can help reduce hyperactive immune responses that fuel inflammatory skin disorders, such as rosacea, eczema, and acne. Additionally, they might boost the innate immune system, which would increase the skin’s resistance to stress [116].

An intact skin barrier is crucial for maintaining hydration and protecting against allergies, infections, and irritants. By encouraging the synthesis of essential structural elements, such as ceramides and tight junction proteins, which close the gaps between skin cells, probiotics can enhance the integrity of the skin barrier [117].

Skin hydration and suppleness can be improved by lowering trans-epidermal water loss (TEWL). Certain strains can alter the pH of the skin, which is crucial for maintaining barrier function and a healthy microbiome [118].

Probiotics compete with harmful microorganisms for adhesion sites and nutrients in the stomach and on the skin. Additionally, they can directly inhibit the growth of harmful bacteria (such as Cutibacterium acne, which is associated with acne, or Staphylococcus aureus, which is frequently linked to eczema) by several methods. Among them is the manufacturing of antibacterial agents [119].

The bacteriocins, hydrogen peroxide, and organic acids (such as lactic and acetic acids) that probiotics can produce make the environment less conducive to the growth of pathogens. Another technique is exclusion from competition. Pathogens are prevented from colonizing and producing biofilms by occupying adhesion sites. The capacity of pathogenic bacteria to coordinate virulence may be hampered by certain probiotics that disrupt their communication networks [120].

Probiotics directly affect skin health by producing a variety of advantageous chemicals (also known as postbiotics) as they break down nutrients: fatty acids with a short chain (SCFA). Butyrate is one of the SCFAs that are produced in the gut and can have systemic anti-inflammatory benefits for the skin [121]. Antioxidants, which help combat free radicals that cause skin aging and damage, can be produced or stimulated by some probiotic strains. Peptides, enzymes (such as sphingomyelinase, which increases the formation of ceramides), and vitamins are a few examples of these that support the health, repair, and rejuvenation of the skin [122].

The combined effects demonstrate how specific probiotic strains can support a balanced skin microbiota and a robust, healthy skin barrier.

Clinical efficacy: Although the effectiveness of probiotics varies significantly depending on the strain used, they show promise in treating skin conditions such as acne and atopic dermatitis (AD). Although outcomes can vary, there is more evidence to support the prevention of AD, especially when it comes to strains like Lactobacillus rhamnosus GG (LGG) in newborns. The process involves building the gut barrier and regulating the immune system [123]. Probiotics, both topical and oral, are becoming more popular as options for acne. By focusing on bacteria like Cutibacterium acnes, they can reduce inflammation, strengthen the skin barrier, balance the skin microbiome, and minimize lesions. According to some research, the outcomes are similar to those of traditional therapies with fewer adverse effects. To determine the optimal strains, dosages, and long-term effectiveness for both illnesses, further study is necessary [124].

Probiotics have shown great potential for skin health, but in order for this research to progress, several important issues need to be resolved. These consist of the following:

Individual reaction variability: The absence of a “one-size-fits-all” solution is a significant obstacle. A probiotic strain that works well for one person may not work at all for another because of the individual differences in microbiome composition, genetics, food, and lifestyle. It is challenging to obtain reliable results because of this high level of inter-individual heterogeneity [125].

Regulatory concerns: Probiotics are frequently categorized as food supplements rather than medications. As a result, they are not held to the same stringent regulatory criteria for production, safety, and efficacy. This may result in the release of goods with unsubstantiated claims, erratic quality, and dosages that differ from those employed in practical studies [126].

Limited clinical trial data: Although early research is promising, there is a lack of extensive, high-caliber clinical trials that provide conclusive evidence for using various probiotic strains for specific skin diseases. To proceed from encouraging connections to well-established therapeutic recommendations, a more thorough study is required to identify the best strains, doses, and treatment durations [127].

3.3. Prebiotics

Definition: Non-digestible compounds that selectively stimulate the growth and/or activity of beneficial microorganisms in the gut. Because of the complex gut–skin axis, prebiotics, including inulin, fructooligosaccharides (FOSs), and galactolactooligosaccharides (GOSs), are important for promoting general health. Their advantages for skin health are also becoming more well-acknowledged.

Prebiotics primarily affect skin health by specifically promoting the development and activity of good bacteria in the stomach. This has several significant effects:

Short-chain fatty acids (SCFAs) such as butyrate, propionate, and acetate are produced as a result of prebiotic fermentation by gut microorganisms. These SCFAs have systemic effects in addition to being essential for gut health. SCFAs may affect the function of the skin barrier and general skin homeostasis, as well as have anti-inflammatory and immune-regulatory effects [128].

Enhance gut barrier: Toxins and undigested food particles are examples of substances that can cause systemic inflammation, and a healthy gut barrier prevents their transport into the bloodstream. Prebiotics encourage the production of chemicals that support gut integrity by feeding beneficial bacteria, which in turn strengthens the gut barrier [129]. Psoriasis, eczema, and acne are examples of inflammatory skin disorders that are frequently associated with a damaged intestinal barrier. Through the enhancement of the gut barrier function, prebiotics may indirectly reduce systemic inflammation, which can manifest as skin problems [116].

Synergy with Probiotics (Synbiotics):

Synbiotics, which combine probiotics and prebiotics, enhance the benefits of both. When probiotics are taken alongside prebiotics (which serve as their “food”), the live beneficial microbes’ ability to survive, thrive, and have positive effects in the gut is increased. A more robust and varied gut microbiota may result from this cooperative relationship, which could enhance the previously mentioned mechanisms and provide a more all-encompassing strategy for promoting skin health from the inside out [130].

3.4. Postbiotics

Non-viable bacterial products or metabolic byproducts generated by probiotic microbes with host-specific biologic activity are known as postbiotics. Postbiotics are useful bioactive substances produced in a matrix during the anaerobic fermentation of organic nutrients, such as prebiotics, to generate adenosine triphosphate, which serves as an energy source. Postbiotics are low-molecular-weight, soluble chemicals that are either secreted by live microflora or released following microbial cell lysis. They are the byproducts of this metabolic sequence. Short-chain fatty acids, microbial cell fragments, extracellular polysaccharides, cell lysates, teichoic acid, vitamins, and other compounds are examples of postbiotics that have been extensively researched [131]. Postbiotics, in particular, have been demonstrated to enhance gut health by bolstering the gut barrier, lowering inflammation, and boosting antimicrobial action against gut pathogens. Moreover, studies are being performed to determine whether postbiotics can be used in the skin, vagina, or oral cavity, among other parts of the body [132].

Advantages: People with damaged skin barriers or weakened immune systems benefit most from postbiotics because they lower the likelihood of infections or negative immunological reactions [133]. Numerous therapeutic actions against vitiligo/hyperpigmentation, rosacea, psoriasis, atopic dermatitis, and acne are among the bioactive qualities. Additionally, it exhibits wound healing, UV-protective, and immunomodulatory qualities. This demonstrates postbiotics’ encouraging therapeutic potential in preserving health and treating skin-related conditions. Because of this, they are especially appropriate for use in topical formulations for those with sensitive or ill skin.

In order to restore microbial balance and increase skin resilience, postbiotics have been added to a range of skincare products, such as cleansers, moisturizers, and serums [134]. Postbiotics have shown promise in treating a variety of skin disorders, including eczema and acne, according to preclinical and clinical research, which supports their use in dermatology. For example, it has been demonstrated that lipoteichoic acid (LTA), a crucial part of the cell wall in Gram-positive bacteria, inhibits melanogenesis [135].

To sum up, the goal of these microbiome-based treatments is to preserve or restore the skin’s microbial communities’ natural equilibrium, which is essential for general skin health. The importance of postbiotics, prebiotics, and other modulators for skin health as well as how they are used in skincare products and treatments was highlighted in the section that followed.

4. Conclusions

The complex and reciprocal interaction between gut microbiota and skin health, known as the gut–skin axis, is crucial for maintaining physiological equilibrium. The skin, the largest organ in the body, plays an active role in many metabolic processes and serves as a crucial barrier and an intricate part of the immune system. Systemic metabolic alterations are among the many internal and environmental factors that have a substantial impact on its integrity and function.

Through its numerous metabolic processes, such as bile acid absorption, xenobiotic detoxification, and the fermentation of dietary fibers into short-chain fatty acids (SCFAs), the gut microbiota plays a crucial role in regulating host health. Maintaining the integrity of the intestinal barrier, regulating immunological responses, and synthesizing vital vitamins all depend on diverse and healthy gut microbiota. Antibiotics, mental stress, and dietary decisions can all cause dysbiosis, a disruption of this delicate balance that can result in systemic inflammation and compromised immunological and metabolic processes, which can then show up as a variety of skin disorders. The relationship between the gut microbiota and its stability is best understood as a dynamic equilibrium, possessing both resilience and a delicate balance. These two concepts are not mutually exclusive; instead, they describe different aspects of how the microbial community responds to various factors.

The historical concept of the gut–skin relationship is being increasingly supported by emerging research. Modern multi-omics techniques validate the impact of gut dysbiosis on immunological responses and systemic inflammation, which, in turn, affect skin homeostasis and disease susceptibility.

Treatment approaches that target the gut microbiota offer promising opportunities to improve skin health. The generation of beneficial SCFAs and the maintenance of a healthy gut environment are facilitated by dietary treatments, particularly those high in fiber. A balanced skin microbiome, enhanced barrier function, and decreased inflammation are all facilitated by prebiotic-rich diets, which also support the growth of healthy gut flora. Additionally, following an anti-inflammatory diet, such as the Mediterranean diet, can reduce systemic inflammation, which can immediately help those with conditions like psoriasis, rosacea, acne, and eczema.

In summary, preventing and treating dermatological disorders necessitates a comprehensive strategy that considers the significant impact of gut microbiota on skin health. To maximize skin health and general well-being, future studies should investigate the intricate interactions within the gut–skin axis and create customized, microbiome-targeted treatments.