Search Results (314)

COVID-19 is associated with gut microbiome alterations that may influence disease outcomes through immune and inflammatory pathways. This systematic review and meta-analysis evaluated global evidence on gut dysbiosis in COVID-19. We searched PubMed/MEDLINE, Embase, Web of Science, Scopus, and Cochrane Library up to 5 October 2025 (PROSPERO CRD420251160970). Alpha-diversity indices and microbial taxa log-fold changes (logFC) were analyzed using random-effects models. The pooled standardized mean difference (SMD) for the Shannon index was −0.69 (95% CI −0.84 to −0.54; I² = 42%), confirming reduced microbial diversity. Faecalibacterium prausnitzii showed a significant pooled depletion (logFC = −1.24; 95% CI −1.68 to −0.80; k = 10; I² = 74%), while Enterococcus spp. was increased (logFC = 1.45; 95% CI 1.12–1.78). Egger’s test did not suggest publication bias (p = 0.32). Gut dysbiosis was consistently associated with reduced microbial diversity and enrichment of pathogenic taxa, correlating with increased disease severity and mortality (HR = 1.67). These findings highlight the potential of microbiome profiling as a prognostic tool in COVID-19, although clinical translation requires further validation. Full article

Background/Objectives: The gut microbiome has an important role in immune regulation, and dietary interventions that support a balanced microbiota may help to prevent the development of allergic asthma. Dietary fibers can beneficially affect the intestinal microbiome, but due to the diversity of fiber types, the effects differ. In this study, we investigate the preventive effects of two mixes of short-chain and long-chain (1:1 and 9:1 ratio) fructo-oligosaccharides (FOS) in a mouse model of house dust mite (HDM)-induced allergic asthma. Methods: BALB/c mice received FOS-supplemented (1% w/w) diets before and during intranasal exposures to HDM. Endpoint airway hyperreactivity measurements were performed, followed by the collection of bronchoalveolar lavage fluid (BALF), lung, serum and cecum content. Fecal microbiome composition was determined by DNA sequencing and short-chain fatty acid (SCFA) levels were determined in the cecum, serum and lung. Results: Fecal microbiome analyses revealed an increased abundance of Prevotellaceae after FOS1:1 supplementation in HDM-allergic mice. Additionally, FOS1:1 protected against an HDM-induced increase in basal airway resistance. Both FOS1:1 and FOS9:1 restored the systemic acetate levels in HDM-allergic mice. The two FOS supplementations did not affect HDM-induced inflammatory cell influx in the BALF. However, FOS1:1 increased the frequency of Th1-cells and prevented an HDM-induced increase in the Th2/Th1 balance. Upon ex vivo restimulation with HDM, lung cell suspensions of FOS1:1-fed mice produced less type 2-related cytokines compared to control-supplemented mice, and FOS9:1 followed a similar pattern. Conclusions: Specific short-chain and long-chain FOS ratios differentially affect the microbiome and immune system in a mouse model with HDM-induced allergic airway inflammation. Dietary supplementation with FOS1:1 shifts the immune response away from type 2, suggesting that dietary fibers like FOS1:1 may contribute as a part of a broader strategy to modulate HDM-induced allergic asthma. Full article

Catheter ablation (CA) has become a validated technique for treating patients with symptomatic or paroxysmal atrial fibrillation (AF), as recommended by the latest 2024 European society of cardiology (ESC) guidelines, class II level A. The procedure is also recommended for patients with persistent AF without major risk factors for AF recurrence, as an alternative to antiarrhythmic medications class I or III. However, CA carries the risk of AF recurrence in 30–35% of patients, sometimes after the procedure. Multiple factors impact the onset, maintenance, and recurrence of AF after CA, including clinical, biohumoral, echocardiographic, genetic, and lifestyle factors. Beyond traditional predictors, emerging factors such as obstructive sleep apnea syndrome, chronic renal failure, chronic lung disease, physical activity patterns, gut microbiota composition, and epicardial fat thickness significantly influence outcomes. Therefore, optimizing patient’s selection for CA is an important strategy to minimize the risk of AF recurrence. Many echocardiographic parameters emerged as predictors of AF recurrence post-CA, but none stood out as a potential single factor. These factors include traditional markers such as left atrial size by 2D echocardiography, LV ejection fraction, LV diastolic function parameters as well as myocardial deformation addressed by the recently developed speckle tracking analysis. Additionally, the duration and type of AF represent fundamental risk factors, with longstanding persistent AF showing significantly higher recurrence rates compared to paroxysmal forms. Novel biomarkers including MR-proANP, caspase-8, hsa-miR-206, and neurotrophin-3 show promise in enhancing risk prediction capabilities. The aim of this review is to explore the most relevant echocardiographic parameters, including myocardial deformation, that could accurately predict recurrence of AF after CA, while also examining the role of emerging clinical and biochemical predictors in comprehensive patient selection strategies. Full article

COVID-19 can cause long-term symptoms, such as a post-infection syndrome, known as Long-COVID. Among the symptoms present during this period, the most reported are gastrointestinal symptoms. This study discusses the effects of changes in the gut microbiota of post-COVID-19 patients. SARS-CoV-2 infection is associated with significant alterations in gut microbial composition, disturbing its homeostasis and promoting a reduction in the abundance of beneficial symbiotic bacteria and an increase in the abundance of opportunistic pathogens. Furthermore, the composition of the gut microbiota may play a role in the prognosis of patients with post-COVID-19 infection. The microbiota of the intestinal tract and the respiratory tract influence each other; therefore, the gut–lung axis has attracted increasing interest in understanding COVID-19. Moreover, the brain–gut axis has been studied, since there have been reports of anxiety and depression along with post-COVID-19 gastrointestinal symptoms. Treatments options for intestinal dysbiosis in Long-COVID patients include probiotics, prebiotics, and fecal microbiota transplantation. These treatments may serve as an approach to improve gastrointestinal symptoms during Long-COVID, increasing microbiome diversity, strengthening the integrity of intestinal barrier functions, and consequently influencing the treatment of COVID-19. Full article

Lung cancer remains the deadliest malignancy, with limited effective and long-term therapeutic options. Immunotherapy has revolutionized the therapeutic landscape of lung cancer. However, not everyone with lung cancer responds to immunotherapy, while, inpatients who temporarily derive clinical benefit, resistance eventually develops. The host microbiome has emerged as a pivotal player in cancer growth and progression. It has been implicated in the intricate connections between immune cells and tumor cells, ultimately augmenting immunotherapy efficacy in solid tumors, while simultaneously mitigating the immune-related adverse events associated with this type of treatment. Notably, lung cancer patients who obtain benefit from immunotherapy have been found to be colonized with specific bacterial populations, and it is this observation that the scientific community is trying to exploit, aspiring to improve lung cancer immunotherapy response rates. Delving deeper into the molecular mechanisms underpinning the effects of the microbiome on immunotherapy is an area that we should pay attention to if we want to utilize microbiome modulation in everyday clinical practice. Fecal microbiota transplantation, probiotics, targeted antibiotic interventions, and dietary modifications are among the strategies that are under investigation in clinical trials, with the ultimate endpoint of lengthening the life expectancy of lung cancer patients. Full article

Micro- and nanoplastics (MNPs) are emerging environmental immunotoxins with widespread human exposure through ingestion, inhalation, and dermal contact. Detected in the placenta, lungs, blood, bone marrow, and brain, MNPs accumulate in immune organs where they disrupt innate and adaptive cell functions. This review aims to provide a comprehensive summary of the current knowledge on how MNPs affect the immune system at the cellular and molecular levels. Experimental evidence shows that MNPs impair macrophage phagocytosis, skew dendritic cell maturation, trigger neutrophil extracellular traps, and alter T and B cell responses. Mechanistically, these effects are driven by oxidative stress, mitochondrial dysfunction, and activation of key inflammatory signaling pathways, including NF-κB, MAPK, and NLRP3 inflammasome, leading to apoptosis, pyroptosis, and chronic low-grade inflammation. Furthermore, MNP-induced disruption of epithelial barriers and gut microbiota composition undermines immune tolerance and contributes to the pathogenesis of autoimmune conditions. Preclinical models provide evidence linking MNP exposure to exacerbation of diseases such as systemic lupus erythematosus, inflammatory bowel disease, and rheumatoid arthritis. However, human epidemiological data remain limited, highlighting the urgent need for standardized exposure protocols, advanced omics technologies, and longitudinal cohort studies are urgently needed to establish causal links and inform public health strategies. Full article

The complexity of adverse responses from radiation injury (RI) followed by physical trauma, namely, radiation combined injury (RCI), is unique and more pronounced than either insult alone due to a poor understanding of the integration of these insults at the molecular/cellular/tissue and/or organ levels. It was shown that mice receiving ⁶⁰Co γ-photon RCI with wounding had a lower LD_50/30 than RI alone. This survival synergism was observed in bone marrow and the gastrointestinal system, as evidenced by an increase in γ-H2AX expression in bone marrow cell DNA, loss of circulatory blood cells, elevation of serum cytokine concentration, and activation of nuclear factor-κB/inducible nitric oxide synthase, and an earlier onset of bacterial infection and sepsis after RCI than after RI was detected. Dysbiosis (imbalance of the gut microbiota) was observed. There remains a pressing need for both prophylactic countermeasures and therapeutic remedies to deal with RCI threats. Investigations of how RCI can affect this important network of communication between the gut microbiota and other organs, including the brain, lung, heart, liver, kidney, and skin, could lead to new and critical interventions and prevention strategies. This review provides an update on new RCI animal models, dynamic changes in cytokine expression, dysbiosis, as well as links between the gut microbiome and other organs after RCI. Full article

Post-COVID-19 syndrome, also known as long-COVID, is characterized by a wide spectrum of persistent symptoms involving multiple body organs and systems, including fatigue, gastrointestinal disorders, and neurocognitive dysfunction. Emerging evidence suggests that gut microbiota dysbiosis and disruption of the gut–brain axis play a central role in the pathophysiology of this condition. Probiotics and their metabolites (postbiotics) have gained increasing attention as potential therapeutic agents given their immunomodulatory, anti-inflammatory, and antiviral properties. In this review, we discuss the current understanding of the antiviral mechanisms of probiotics, including reinforcement of intestinal epithelial barrier function, direct virus inhibition, receptor competition, and immune system modulation. Special emphasis is placed on short-chain fatty acids (SCFAs), lactic acid, hydrogen peroxide, and bacteriocins as key factors that contribute to these effects. SCFAs appear to be essential postbiotic compounds during post-COVID recovery. We also highlight recent clinical trials involving specific probiotic species, such as Lactiplantibacillus plantarum, Lacticaseibacillus rhamnosus, and Bifidobacterium longum, and their potential role in alleviating long-term COVID symptoms. Although the current results are promising, further research is needed to clarify the most effective strains, dosages, and mechanisms of action in post-COVID therapeutic strategies. Full article

Long COVID, also referred to as post-acute sequelae of SARS-CoV-2 infection (PASC), is characterized by persistent multi-systemic symptoms such as fatigue, cognitive impairment, and respiratory dysfunction. Accumulating evidence indicates that gut and oral microbiota play an important role in its pathogenesis. Patients with long COVID consistently exhibit reduced microbial diversity, depletion of beneficial short-chain fatty acid (SCFA)-producing species such as Faecalibacterium prausnitzii and Bifidobacterium spp. and enrichment of proinflammatory taxa including Ruminococcus gnavus, Bacteroides vulgatus, and Veillonella. These alterations may disrupt intestinal barrier integrity, sustain low-grade systemic inflammation, and influence host immune and neuroendocrine pathways through the gut–brain and gut–lung axes. Distinct microbial signatures have also been associated with symptom clusters, including neuropsychiatric, respiratory, and gastrointestinal manifestations. Proposed mechanisms linking dysbiosis to long COVID include impaired SCFA metabolism, tryptophan depletion, microbial translocation, and interactions with host immune and inflammatory responses, including autoantibody formation and viral antigen persistence. Preliminary interventional studies using probiotics, synbiotics, and fecal microbiota transplantation suggest that microbiome-targeted therapies may alleviate symptoms, although evidence remains limited and heterogeneous. This review synthesizes current literature on the role of gut and oral microbiota in long COVID, highlights emerging microbial biomarkers, and discusses therapeutic implications. While causality remains to be firmly established, restoring microbial balance represents a promising avenue for diagnosis, prevention, and management of long COVID. Full article

Atopic dermatitis (AD) and asthma are key manifestations of the atopic march, characterized by a progressive development of allergic diseases from early skin inflammation to later respiratory involvement. Emerging evidence highlights the role of gut microbiota in modulating immune responses. However, the therapeutic potential of specific probiotic strains in preventing or mitigating the atopic march remains underexplored. This study aimed to evaluate the immunomodulatory and therapeutic effects of selected probiotic strains in a murine model of ovalbumin (OVA)-induced AD and asthma. Mice received oral administration of B. plebeiu, B. ovatus, F. duncaniae, F. taiwanense, and F. prausnitzii for four weeks before being exposed to OVA to induce AD and, later, asthma. Skin reactions were assessed after OVA application, and asthma was induced via aerosolized OVA. Afterward, blood and lung fluid samples were collected to evaluate immune markers such as total IgE, OVA-specific IgE, and IL-4. The results showed that B. plebeius improved skin histology in AD, while B. ovatus initially induced AD symptoms but later reduced them significantly between days 40 and 54. B. plebeius and B. ovatus reduced serum total IgE in asthma. B. plebeiu, B. ovatus, F. duncaniae, F. taiwanense, and F. prausnitzii significantly lowered OVA-IgE levels in serum and IL-4 levels in lung fluid (p < 0.05). These selected probiotic strains helped reduce allergic skin responses and, later, asthma by decreasing inflammation, particularly IL-4. These findings support the potential of these probiotics to prevent or mitigate the progression from AD to asthma and offer promising insight into targeted probiotic interventions for allergic diseases. Full article

Background: Acute lung injury (ALI) is a life-threatening respiratory condition and one of the leading causes of mortality worldwide, accounting for approximately 20% of global annual deaths. Despite its high prevalence and severity, effective therapeutic options remain limited. Eupatorium lindleyanum DC., a traditional medicinal herb, has demonstrated therapeutic potential against pulmonary diseases, particularly ALI, in both clinical and experimental settings. However, the protective effects and underlying mechanisms of its characteristic sesquiterpene lactone components against ALI remain unclear. Objective: This study aimed to evaluate the protective effects of sesquiterpene lactones from Eupatorium lindleyanum DC. (SLEL) against lipopolysaccharide (LPS)-induced ALI both in vivo and in vitro. Furthermore, it sought to elucidate the underlying mechanisms by integrating network pharmacology, multi-omics approaches (transcriptomics, metabolomics, and 16S rRNA sequencing), and various molecular biology techniques. Results: SLEL significantly attenuated inflammatory injury in alveolar epithelial cells and alleviated pulmonary edema, hemorrhage, and inflammatory infiltration in rats, accompanied by reduced TNF-α, IL-6, and IL-1β levels and improved lung injury indices. Mechanistically, SLEL exerted dual suppression of the PI3K-Akt and MAPK-NF-κB pathways. Network pharmacology, molecular docking, and UPLC-MS analyses identified Eupalinolide A and Eupalinolide K as potential bioactive constituents, which were further validated to inhibit phosphorylation of key signaling proteins, thereby partially accounting for SLEL’s pharmacological effects. Multi-omics integration further revealed that SLEL restored bile acid metabolism, reshaped gut microbial diversity, and reconstructed the microbiota–metabolite–inflammatory cytokine network, thereby maintaining gut–lung axis homeostasis and enhancing anti-inflammatory effects. Conclusions: SLEL alleviates ALI through multi-component synergistic actions that suppress pro-inflammatory signaling and modulate the gut–lung axis. These findings highlight the potential of SLEL as a promising therapeutic candidate for the treatment of ALI. Full article

Obesity and asthma are increasingly prevalent chronic conditions that often coexist in the pediatric population and may influence each other through shared pathophysiological mechanisms. Obesity can affect asthma expression and severity via mechanical effects on the lungs, systemic inflammation, altered adipokine levels, and metabolic dysregulation. These mechanisms contribute to a distinct asthma phenotype in children with obesity that is often less responsive to standard therapy. Nutrition plays a critical role in this context by influencing immune function, inflammation, and respiratory outcomes. Specific dietary patterns, such as the Mediterranean diet, along with nutrients including vitamin D, antioxidants, and polyunsaturated fatty acids, have been associated with the modulation of airway inflammation and asthma risk. Additionally, early-life nutritional exposures and gut microbiota composition may influence immune development and the propensity for allergic diseases. This narrative review aims to synthesize current evidence on the interplay between obesity, asthma, and nutrition in the pediatric population, highlighting potential dietary interventions and targets for improved asthma management in children with obesity. Full article

Background: Lung cancer is the leading cause of cancer-related mortality globally, with lung adenocarcinoma (LUAD) as the most common subtype. Dysbiotic intratumoral mycobiomes drive LUAD pathogenesis, and Aspergillus sydowii (A. sydowii) acts as a key oncogenic fungal species. Ginseng polysaccharides (GPs), bioactive phytochemicals with immunomodulatory and oncostatic properties, counteract fungal infections and restore immunosurveillance in LUAD. Methods: Subcutaneous and orthotopic LUAD murine models were established by implanting Lewis lung carcinoma (LLC) cells. Subcutaneous tumors were infected intratumorally and orthotopic models via nasal inoculation. GPs (200 mg/kg/day) were orally administered to evaluate tumor growth. Metagenomic and targeted bile acid metabolomic profiling of fecal and tumor tissues was performed, with Spearman correlations analyzed using R packages. Results: GPs significantly inhibited A. sydowii-induced tumor growth in both models. In subcutaneous tumors; GPs reduced volume (p < 0.05) and weight vs. infected controls. In orthotopic models, GPs decreased pathological nodules and lung weight, with micro-CT/H&E confirming attenuated hyperplasia. Metagenomics showed GPs restored gut homeostasis by enriching Lactobacillus/Muribaculum intestinale and suppressing pro-inflammatory Alistipes. Targeted metabolomics revealed reduced β-Hyodeoxycholic Acid (3β-HDCA), Chenodeoxycholic acid 24-acyl-b-D-glucuronide (CDCA-24G) and 3β-hydroxychol-5-en-24-oic acid (5-isoLCA) after GP treatment. Network analysis confirmed significant microbe–bile acid interactions. Conclusions: GPs exert antitumor effects against A. sydowii-induced LUAD by modulating gut microbiota and bile acid metabolism. This identifies GPs as a promising therapy for mycobiome-influenced cancers, with dual targeting of fungal infection and metabolic reprogramming. Full article

Micro- and nanoplastics (MNPs) are emerging environmental contaminants with increasing evidence of bioaccumulation in human tissues and potential toxicological effects. While extensive studies in the literature have investigated MNP exposure and health risks in adult populations, data specific to pediatric age remain scarce and fragmented. This narrative review represents the first integrated synthesis of current evidence on MNP exposure during early life, including the critical period of the first 1000 days, examining routes of absorption (oral, inhalational, dermal, and iatrogenic), biological distribution, and organ-specific effects in infants and children. Special attention is given to the presence of MNPs in pediatric lungs, thyroid, and intestinal microbiota, as well as to emerging non-invasive biomarkers for exposure assessment. The developing physiology of children, characterized by immature detoxification systems, critical windows of vulnerability, and prolonged life-course exposure, amplifies concern for long-term health consequences, including endocrine disruption, immune dysregulation, and neurodevelopmental impairment. This work fills a critical knowledge gap by consolidating pediatric data into a single comprehensive resource, and it is intended to serve both as a reference point for clinicians and researchers and a catalyst for future studies aimed at safeguarding child health in an increasingly plastic-contaminated world. Full article

Intracellular oxidation–reduction (redox) potential is a key factor regulating various physiological phenomena in the cell. Monitoring this potential change is therefore important for understanding physiological homeostasis in cells. Herein, we propose a new approach for the real-time, non-invasive estimation of the redox potential impacting biological metabolism and reactive oxygen species generation. Enzymes, specifically oxidoreductases, play a crucial role in catalyzing redox reactions by facilitating the transfer of electrons and hydrogen atoms between molecules. The redox potential of substrates, such as nicotinamide adenine dinucleotide, is determined by the ratio of its oxidized and reduced forms, while that of enzymes, such as succinate dehydrogenase, is determined using the reference electrode in protein-film voltammetry. Although the standard hydrogen electrode potential is defined as zero under standard conditions, the electrode potential of a reversible hydrogen electrode changes according to the ratio of the hydrogen ions (H⁺) and hydrogen gas (H₂) in the biological fluids, as a reference electrode. The pH is maintained at 7.4 ± 0.1 in the arterial blood and the H₂ that produced by the gut microbiota is measured in the endo-tidal breath for clinical diagnosis. The H₂ in the endo-tidal breath equilibrates arterial blood during gas exchange in the lungs, as well as in whole-body tissues, due to the systemic circulation. In this study, H₂ can be measured in the environmental gas compared to the atmosphere, and may serve as a novel factor for redox potential changes in redox enzymes, impacting biological metabolism and reactive oxygen species generation. Full article