Search Results (170)

Deoxynojirimycin (DNJ), the first isolated iminosugar, is a natural alkaloid acting as a potent inhibitor of α-glucosidase with high nutritional value. It naturally occurs in plants (especially Morus spp.), microbes, and insects or can be synthesized. Diverse biological activities, such as antihyperglycemic, lipid-lowering, antitumor, antiviral, and anti-inflammatory, have been recognized for this compound. However, DNJ has not been approved as a food supplement until now. Several studies, also in clinics, are carried out on Morus spp. containing DNJ. Among Morus spp., Morus alba L. (white mulberry), Morus nigra L. (black mulberry), and Morus rubra L. (red mulberry) are the three main species that grow all over the world. Some spurious studies have been conducted on Reducose^® and Glubloc™, two products that contain DNJ and Morus alba, respectively. However, mulberry allergy, including respiratory allergy, airborne contact urticaria, anaphylaxis, oral allergy syndrome, and food induced urticaria, may be observed. This review aims to explore a crucial and timely question: how DNJ exerts its biological effects and what role it may play in therapeutic applications. We provide a comprehensive summary of the current understanding of DNJ’s pharmacological potential and the methods used for its production. We also report recent developments in clinical studies on Morus alba, Reducose^® and Glubloc™. Full article

Background: The escalating prevalence of food allergies, alongside the global call for environmentally sustainable dietary transitions, has drawn attention to plant-based dietary models—particularly those inspired by the EAT-Lancet Commission. These frameworks not only reduce reliance on animal-sourced foods, benefiting planetary health, but may also play a role in modulating immune tolerance and allergic responses. Methods: This scoping review followed PRISMA guidelines and included 53 peer-reviewed studies published between 2000 and 2024, retrieved from PubMed, Scopus, and Google Scholar. Eligible articles were classified into two thematic domains: prevention of food allergy onset (n = 31) and modulation of allergic symptoms in sensitized individuals (n = 22). Included studies comprised randomized controlled trials (n = 6), observational studies (n = 17), systematic reviews and meta-analyses (n = 11), and narrative/scoping reviews (n = 19). Results: Sustainable plant-based diets were consistently associated with a lower incidence of allergic sensitization and reduced symptom severity. These effects were partly due to the exclusion of common allergens (e.g., dairy, eggs, and shellfish) but more importantly due to immunomodulatory mechanisms. Fermentable fibers can enhance short-chain fatty acid (SCFA)-producing bacteria (e.g., Faecalibacterium prausnitzii), elevating butyrate and acetate levels, which interact with G-protein-coupled receptors 43 and 109A (GPR43 and GPR109A) to induce regulatory T cells (Tregs) and reinforce epithelial integrity via tight junction proteins such as occludin and claudin-1. Polyphenols (e.g., quercetin and luteolin) can inhibit Th2-driven inflammation by stabilizing mast cells and downregulating IL-4 and IL-1. Conclusions: Following sustainable dietary guidelines such as those proposed by the EAT-Lancet Commission may confer dual benefits: promoting environmental health and reducing the burden of allergic diseases. By emphasizing plant-based patterns rich in fiber and polyphenols, these diets support microbiota-mediated immune education, mucosal barrier function, and immunological tolerance. When properly supervised, they represent a promising tool for allergy prevention and symptom management. Larger randomized trials and long-term population studies are needed to confirm and operationalize these findings in clinical and public health contexts. Full article

Seafood (fish, crustacean, and mollusk) allergy represents a critical global health issue. Food processing offers a viable strategy for allergenicity mitigation and serves as a critical intervention for seafood allergy prevention. This paper reviews recent advances in seafood allergen research, with particular focus on molecular properties, epitopes, and structure–allergenicity relationships, which are foundations for designing processing technologies to mitigate allergenicity. Furthermore, an analysis of how various food processing techniques modulate allergen structures and epitopes, ultimately affecting their allergenicity, was conducted. Current World Health Organization (WHO)/International Union of Immunological Societies (IUIS) listings include 44 fish allergens and 60 shellfish allergens, with their characterization enabling targeted processing approaches for allergenicity elimination. Physical processing techniques, including thermal and non-thermal treatment, can dramatically influence the conformational and linear epitopes by altering or destroying the structure of an allergen. Chemistry-based processing techniques (enzymatic-catalyzed cross-linking and glycation), which induce covalent/non-covalent interactions between allergens and various modifiers, can effectively mask epitopes through molecular complexation. Biological processing attenuates allergenicity by inducing protein unfolding, polypeptide chain uncoiling, and enzymatic degradation. Nevertheless, the structure–activity relationship of seafood allergens remains insufficiently elucidated, despite its critical role in guiding processing technologies for allergenicity elimination and elucidating the fundamental mechanisms involved. Full article

Non-steroidal anti-inflammatory drugs (NSAIDs) can cause hypersensitivity reactions and lead to anaphylactic shock. These drugs also act as cofactors in allergic reactions. Lipid transfer proteins (LTPs), found in plants, represent a unique group of allergens in which cofactors play a crucial role. This case report describes a 26-year-old female who developed anaphylactic symptoms after ingesting grapes and taking ketoprofen. The patient experienced swelling of the lips, tongue, and throat, as well as shortness of breath, dizziness, and loss of consciousness, after consuming grapes and taking ketoprofen. She had previously used ketoprofen and acetylsalicylic acid without issues but had developed urticaria on several occasions after consuming multi-ingredient dishes. Skin prick tests showed positive results for peanut and orange allergens. Further testing using the ALEX multiparametric test detected antibodies to several LTP allergens. Intradermal tests with ketoprofen yielded a positive result, although irritant reactions could not be ruled out. A provocation test with acetylsalicylic acid (ASA) showed no adverse reactions. Skin tests with ibuprofen were negative, and provocation tests confirmed its tolerance. A diagnosis of LTP allergy and selective ketoprofen allergy was made, with the recommendation to avoid ketoprofen and follow a diet excluding foods from the LTP group. Full article

Food allergies result from dysregulated immune responses to dietary antigens. IgE antibodies are key in triggering allergic reactions through binding to high-affinity receptors on mast cells and triggering mast cell activation when crosslinked by allergens. In contrast, IgG antibodies—particularly IgG4—are linked to immunomodulation and tolerance. Allergen-specific memory B cells, especially IgG1+ cells, undergo class-switching to IgE, and IgE plasma cells underlie allergy persistence. Although there is no cure, allergen-specific immunotherapy (AIT) aims to achieve sustained unresponsiveness by gradually increasing allergen exposure. Oral immunotherapy (OIT), a form of AIT, induces a shift from a TH2-skewed response to a more regulated immune profile, characterized by a switch from IgE to IgG4 and IgA isotypes. This review outlines current insights into AIT’s cellular and humoral mechanisms, with implications for improving long-term outcomes and developing predictive biomarkers. Full article

Background and aim: Neurobehavioral changes associated with food allergies have been reported, but the therapeutic effects of probiotics have not been fully explored. Our study aimed to investigate the impact of multi-strain probiotics on neurobehavioral outcomes and to elucidate the underlying mechanism via the microbiota-gut-brain axis. Methods: C57BL/6J Male mice were randomly divided into the following three groups: (1) control group; (2) OVA-sensitized group; (3) OVA-sensitized group treated with multi-strain probiotics (OVA + P). Anaphylactic reactions and behavioral abnormalities were assessed by histological, immunological, and behavioral analyses. To further elucidate the underlying mechanisms, the prefrontal cortex was collected for microglial morphological analysis, while serum and fecal samples were obtained for untargeted metabolomic profiling and 16S rDNA-based gut microbiota analysis, respectively. Results: Multi-strain probiotics significantly alleviated anaphylactic reactions in OVA-sensitized mice, as evidenced by reduced serum IgE levels, decreased Th2 cytokines, and reduced epithelial damage. Meanwhile, neurobehavioral symptoms were alleviated, including anxiety-like and depression-like behaviors, repetitive behaviors, social avoidance, and impaired attention. Mechanistically, probiotics administration suppressed production of inflammatory cytokines (TNF-α, IL-1β and IL-6) and inhibited activation of M1 microglia in the prefrontal cortex, which might contribute to neuron recovery. Furthermore, multi-omics analysis revealed that amino acid metabolism restoration in OVA + P mice, particularly carboxylic acids and derivatives, which was remarkably correlated with alterations in gut microbiota and behaviors related to FA. Conclusions: Gut microbiota and its amino acid metabolites mediate the therapeutic effects of multi-strain probiotics on FA-induced behavioral abnormalities. These effects occur alongside the suppression of neuroinflammation and microglial activation in the prefrontal cortex. Our findings highlight the neuroimmune regulatory role of the gut-microbiota-brain axis and support the potential use of probiotics as an intervention for FA-induced brain dysfunctions. Full article

Food-Induced Immediate Response of the Esophagus (FIRE) is a newly described syndrome observed in eosinophilic esophagitis (EoE) patients. It is defined by an immediate hypersensitivity reaction of the esophagus that occurs when specific foods and beverages interface with esophageal mucosa. The available data regarding this topic is scarce. Therefore, we aimed to review relevant publications in order to better characterize the main aspects of this syndrome and hypothesize about potential mechanisms underlying FIRE syndrome and possible future therapeutic approaches. We searched PubMed, Embase, and Web of Science databases for relevant articles published before February 1st, 2025. The results were narrowed down to four articles describing a total of 105 cases of FIRE syndrome. These patients had a distinct clinical presentation, characterized by retrosternal discomfort or pain, differentiating it from solid food dysphagia or pollen-food allergy syndrome (PFAS). Currently, diagnosis is based on clinical presentation, with no diagnostic tests or biomarkers available. Emerging evidence suggests that IgE-mediated hypersensitivity, mast cells, and neuroimmune interactions may play a central role in the pathogenesis of FIRE syndrome. The therapeutic approaches remain speculative, with trigger avoidance being the main option. This article brings to the forefront the need for continued research to address current knowledge gaps regarding FIRE syndrome, which is important for optimizing patient management. Full article

Background: Cow-milk-induced allergic proctocolitis (CMIAP) is a non-IgE-mediated food hypersensitivity that often resolves spontaneously but may predispose infants to IgE-mediated allergies and eosinophilic gastrointestinal disorders. Understanding its pathophysiology is crucial for microbiota-based interventions. Methods: We enrolled 32 exclusively breastfed infants—16 with confirmed cases of CMIAP and 16 age-matched healthy controls. The cohorts were sex-balanced (8 F/8 M), term-born (gestational age ± SD: 40 ± 1.2 vs. 39 ± 1.3 weeks), vaginally delivered, and sampled at a mean age of 2.0 ± 0.44 months (range 1.5–3.0) vs. 2.4 ± 0.66 months (range 1.5–3.5). Faecal samples underwent 16S rRNA gene sequencing on the Illumina NovaSeq platform, with diversity and differential abundance analyses. Results: The maternal dairy intake was similar (total dairy: 250 ± 80 vs. 240 ± 75 mL/day; yoghurt: 2.3 ± 1.0 vs. 2.5 ± 1.2 days/week; p = 0.72). Bray–Curtis dissimilarity assessments revealed distinct microbiota in infants with CMIAP. Infants with CMIAP had a lower abundance of Bifidobacterium (log₂FC−2.27; q = 0.022; ANCOM-BC), Collinsella (−29.35; padj < 0.0001; DESeq2), and Limosilactobacillus (−8.01; padj = 0.0285; DESeq2; q < 0.0001; ANCOM-BC) compared with controls. In contrast, Hungatella (+24.99; padj < 0.0001; DESeq2), Veillonella (+4.73; padj = 0.0221; DESeq2), Citrobacter (+10.44; padj = 0.0124; DESeq2), and Ruminococcus gnavus (+2.69; q < 0.0001; ANCOM–BC) were more abundant in the CMIAP group. Conclusions: Infants with CMIAP exhibit gut dysbiosis, which is characterised by the depletion of beneficial commensals and the enrichment of potential pathogens, independent of maternal dairy intake. Further studies should establish whether these microbiota alterations are causal or consequential in CMIAP. Full article

Food colourants are widely used additives classified as either synthetic or natural. In recent years, consumers have increasingly favoured natural options, considering them safer and potentially beneficial due to their nutritional properties. This study examined the effects of a natural food colourant, commercially known as Vegan Red (RVEG), on zebrafish embryonic development. Its impact was compared with cochineal red E120, of animal origin, and the synthetic dye E124, which are associated with hyperactivity in children and allergies. Shield stage embryos were exposed for 72 h and then examined using a multidisciplinary approach to assess the effects on conventional toxicity endpoints, such as survival, hatching rate, heart rate, genotoxicity, and behavioural interferences, including the impact on muscle ultrastructure. The results demonstrated that RVEG, as well as E120, do not affect hatching, heart rate, and motility parameters. However, RVEG moderately alters skeletal muscle organisation and, more relevant, the expression of the gfap, chchd2, and notch1a genes. Based on standard toxicity parameters, the findings indicated that RVEG is less toxic than E124 and E120, but that the alterations induced in gene expression and muscle anatomy raise safety concerns. Full article

A close association between obesity and food allergies has been described, but from the perspective of T cell differentiation, controversial findings exist regarding the impact of high-fat diet (HFD) feeding on the development of food allergies. Our study aimed to explore the relationship between HFD-induced mild obesity and food allergy development in female BALB/c mice. Following 18 weeks of HFD feeding, experimental animals demonstrated a 10.92% body weight gain accompanied by a 32.45% elevation in total cholesterol levels and a 39.50% increase in low-density lipoprotein–cholesterol levels. Upon allergen challenge, control diet (COD)-fed mice developed obvious food allergy symptoms and hypothermia, which were slightly alleviated in HFD-fed mice. Flow cytometry revealed that splenocytes from HFD-fed mice exhibited a 102.32% increase in CD4⁺T-bet⁺ T (Th1) cell populations and a 38.69% elevation in CD4⁺RORγt⁺ T (Th17) cell populations compared to COD-fed allergic mice. These changes corresponded with a 28.41% reduction in the Th2/Th1 ratio and a 56.67% increase in the Th17/Treg ratio. Moreover, real-time quantitative PCR showed that HFD-fed allergic mice had higher expressions of Foxp3, Occludin1, and TJP1 in the intestine. Therefore, we concluded that HFD-induced mild obesity restored the Th2/Th1 and Th17/Treg balance, reinforced intestinal barrier function, and thereby did not increase allergy risk in female BALB/c mice. Full article

The neurobehavioral changes in food allergy mice have not been comprehensively studied, and the mechanism underlying them remains unclear. Our study aims to fully investigate neurobehavioral changes in OVA (ovalbumin)-sensitized food allergy mice and explore the potential mechanism via the gut microbiota–brain axis. We established the food allergy mouse (C57BL/6J male) model with OVA, evaluating the anaphylactic symptoms and the levels of Th2 signature cytokine and allergy-related antibodies in serum. Using behavioral tests, we measured anxiety, depression, social behavior, repetitive behavior, attention, and spatial memory in control and OVA mice. In addition, we analyzed the prefrontal cortex for measuring inflammation-related indicators and gathered serum for untargeted metabolomics analysis and feces for 16S rDNA sequencing. OVA mice exhibited anaphylactic symptoms and significantly elevated serum IgE and Th2 signature cytokine levels. In addition to anxiety-like, depression-like, and repetitive behaviors, OVA mice also displayed less social interest and damaged attention. TNF-α, IL-1β, and IL-6 levels and the activation of microglia in the prefrontal cortex of OVA mice were significantly increased, which might explain the neuronal damage. Using multi-omics technology, amino acid metabolism disruption, particularly carboxylic acids and derivatives, was observed in OVA mice, which was remarkably correlated with the altered abundance of gut microbiota related to food allergy. Behaviors in OVA-induced food allergy mice were extensively impaired. The disruption of amino acid metabolism associated with gut microbiota dysbiosis in OVA mice might play a pivotal role in impairing neural immune homeostasis and neuronal damage, which could be responsible for behavioral abnormalities. Full article

Background: Ovalbumin (OVA) is a major allergen in egg whites. Introduction: Given the crucial role of gut microbiota in OVA-induced allergy, it remains unclear whether gut microbiota could serve as a therapeutic target for OVA allergy prevention. Method: To investigate the relationship between gut microbiota and food allergy, a two-sample bidirectional Mendelian randomization approach was combined combined with gut microbiota diversity analysis in vivo. Statistical analysis was performed, with p < 0.05 considered statistically significant and p < 0.01 highly significant. Results and discussion: Notably, Lachnospiraceae represents a potential therapeutic target for food allergy intervention, but the discrepancy between the MR and experimental findings highlights the limitations of the current research. When targeting the genus Lachnospiraceae, we observed that narirutin administration increased the abundance of the family Lachnospiraceae and the genus Lachnospiraceae_NK4A136_group. Conclusions: Narirutin may exert protective effects by increasing Lachnospiraceae abundance, but its precise mechanism—particularly whether it depends on SCFAs—requires further investigation. Full article

Background: Food allergy (FA) poses a major global health issue due to the increasing prevalence and lack of effective prevention strategies. Allergen-specific immunotherapy (AIT) has emerged as a disease-modifying therapy for FA. However, due to long-term treatment duration and unexpected adverse reactions, only a minority of patients benefit from AIT. Therefore, effective prophylactic interventions are urgently needed for FA patients. Methods: In this proof-of-concept study, using a well-established mRNA platform, we developed mRNA vaccine candidates encoding for the major egg white allergen Gal d2 and comprehensively evaluated their prophylactic efficacy against anaphylaxis in a Gal d2-induced allergic mouse model. Results: Two vaccine formulations, Gal d2 mRNA vaccine and Gal d2-IL-10 mRNA vaccine, both demonstrated potent ability in inducing allergen-specific IgG and Th1-type T cells. Importantly, the two vaccine formulations showed promise in preventing the onset of allergic disease, which is indicated by prevention of body temperature decline during anaphylaxis. Conclusions: We provided preliminary proof-of-concept evidence showing that the mRNA platform is unique and holds promise for the development of anti-allergy vaccines. This is largely attributed to the capacities of mRNA vaccines in eliciting an allergen-blocking antibody, shifting Th2 towards Th1 immunity, as well as in generating peripheral tolerance. However, further investigations are required to better understand the mode of action. Full article

Oral immunotherapy (OIT) is a promising approach for treating food allergy. Here, we elucidated the mechanisms of desensitization induced by OIT in rats sensitized to ovalbumin (OVA). The desensitization was induced by ingestion of OVA three times per week after sensitization in rats. OIT suppressed the decrease in rectal temperature and increase in plasma histamine levels induced by OVA injection immediately and 4 weeks after OIT completion. Plasma OVA-specific IgE (sIgE) levels did not differ between the non-OIT and OIT groups, but OVA-specific IgG₁ levels were higher in the OIT group than in the non-OIT group at both timepoints. To evaluate IgG’s effect on IgE crosslinking with OVA, amplified luminescence proximity homogeneous assay involving crosslinking (AlphaCL) was performed. When IgG was removed using a Protein G column, the AlphaCL signal was significantly increased, especially in the OIT group, indicating that OIT-induced IgG inhibited the sIgE response. The proportions of cluster of differentiation (CD)4⁺ cells and CD4⁺CD25⁺FoxP3⁺ cells in mesenteric lymph nodes and spleen were similar between the two groups. These findings indicate that OIT attenuates systemic allergic responses by inhibiting sIgE binding to OVA through increased IgG. Our model is useful for understanding the mechanisms of OIT and optimizing therapeutic strategies for ameliorating food allergies. Full article

Acute and chronic Food Protein-Induced Enterocolitis Syndrome (FPIES) has been well characterized in children; otherwise, neonatal FPIES (N-FPIES) remains poorly understood. In terms of pathophysiology, neonatal FPIES appears to have a more prevalent TH2 response and is characterized by specific clinical features that make the diagnosis challenging. Genetic and environmental risk factors may predispose to the development of FPIES. Recent evidence indicates that a characteristic microbiota signature may lead to barrier dysfunction, reduced regulatory T cells, and abnormal intestinal production of serotonin, responsible for the symptoms of FPIES. Regarding clinical presentation, newborns with FPIES may not fully meet the current guideline’s diagnostic criteria at disease onset, being more similar to clinical entity specific of neonatal age than to acute FPIES in infants and children. Hence, differentiation from other neonatal medical and surgical conditions—particularly necrotizing enterocolitis (NEC)—remains a critical challenge for clinicians. This present review highlights our current understanding of N-FPIES, in term of pathophysiology, clinical presentation diagnosis, and treatment strategies. Refining diagnostic criteria for N-FPIES represents a clinical priority to help physicians in diagnosing and managing this challenging condition. Last, but not least, larger clinical trials are needed to optimize treatment practices in term and preterm newborns with FPIES. Full article