Growing evidence indicates that the gut microbiota is a central regulator of systemic immunity, acting through epithelial barrier integrity, microbial metabolites, and bidirectional signaling with innate and adaptive immune cells. Within this framework, probiotics have attracted substantial interest as tools for immune modulation; however, their effects are not uniform and should not be generalized across species or formulations. This review synthesizes current evidence on the gut microbiota–immune axis and examines how defined probiotic strains influence immune homeostasis, inflammation, and clinical outcomes. Particular emphasis is placed on strain-specific effects among lactic acid bacteria, bifidobacteria, yeast probiotics, and emerging nontraditional candidates, with attention to mechanisms involving cytokine signaling, regulatory T-cell induction, nuclear factor kappa B (NF-κB) modulation, toll-like receptor (TLR) pathways, short-chain fatty acids (SCFAs), tryptophan metabolites, and bile-acid-dependent signaling. The available literature indicates that the most meaningful immunological effects arise from precisely characterized strains acting in specific host contexts, whereas inconsistent trial design, small sample sizes, variable dosing, and poor strain resolution continue to limit translation. Overall, current data support a shift from generic probiotic use toward mechanism-based, strain-specific, and increasingly personalized strategies for immune modulation.

Non-celiac villous atrophy (NCVA) is a multifaceted and under-recognized clinical entity with an etiology beyond celiac disease. This review critically examines the diverse pathophysiological mechanisms underlying NCVA, including autoimmune enteropathies, immune deficiency-related disorders, infectious processes, drug-induced trauma, and metabolic or environmental influences. A comprehensive synthesis of peer-reviewed literature, clinical studies, and case reports was conducted, adopting a multidisciplinary perspective that integrates immunologic, infectious, metabolic, and pharmacologic insights. The literature search was performed in three phases: identification of relevant studies, critical assessment of selected publications, and synthesis of key findings. Searches were carried out in PubMed, Scopus, Web of Science, and Google Scholar databases. The final search, completed in June 2025, included international, English-language articles, electronic books, and online reports. Studies were included if they addressed NCVA in the context of pathophysiology, clinical manifestations, or management strategies, with priority given to publications from the last ten years (2015–2025). The search strategy used the primary term “non-celiac villous atrophy” combined with supplementary keywords such as autoimmune enteropathy, common variable immunodeficiency, tropical sprue, drug-related enteropathy, pathophysiology, immunological mechanisms, chronic inflammation, genetic factors, environmental influences, and clinical management. Histopathological evaluations reveal that NCVA often manifests with varying degrees of villous blunting, crypt hypertrophy, and intraepithelial lymphocytosis, albeit without the gliadin-specific immune response seen in celiac disease. Various immune pathways are involved, such as autoimmune deregulation and chronic inflammatory responses, while drug-induced and environmental factors further complicate its clinical picture. These findings highlight significant diagnostic challenges and underscore the need to adapt diagnostic algorithms that combine clinical history, serologic evaluations, and histopathologic analysis. In conclusion, an in-depth understanding of the heterogeneous etiology of NCVA is critical to improving diagnostic accuracy and optimizing therapeutic strategies. Future research should prioritize the identification of specific biomarkers and the development of targeted interventions to address the unique mechanisms underlying NCVA, thereby improving patient management and outcomes.

The human gastrointestinal tract hosts a complex ecosystem known as the gut microbiota, which plays a crucial part in digestion and immune system function. Among the clinically recognized manifestations of dysbiosis in this system are Small Intestinal Bacterial Overgrowth (SIBO), Intestinal Methanogen Overgrowth (IMO), Small Intestinal Fungal Overgrowth (SIFO), and Large Intestinal Bacterial Overgrowth (LIBO). This study aims to investigate the complex pathophysiological mechanisms underlying these syndromes and their diagnostics and therapeutic options, focusing primarily on the roles of methane-producing archaea and fungal overgrowth. The methods employed in this study involve a comprehensive analysis and synthesis of peer-reviewed articles, systematic reviews, clinical trials, and meta-analyses. This review summarizes that methane production by Methanobrevibacter smithii was linked to altered fermentation, reduced microbial diversity, and slowed intestinal transit. Fungal species were associated with increased intestinal permeability, inflammation, and biofilm formation. Targeted interventions addressing microbial imbalances demonstrated potential therapeutic value. This review highlights the complex and multifactorial nature of gut dysbiosis, revealing its impact beyond the gastrointestinal tract. While emerging therapies targeting methanogens, fungi, and biofilms show promise, further research is essential to optimize their clinical application. The findings emphasize the need for interdisciplinary collaboration to refine diagnostic and therapeutic strategies.

Eosinophilic esophagitis (EoE) is a chronic, food-driven inflammatory disorder of the esophagus in which repeated exposure to dietary antigens plays a central role, yet identification of clinically relevant food triggers remains largely empirical. In this retrospective, single-center study, molecular IgE sensitization profiles were descriptively characterized in adult patients with EoE (n = 22) and compared with an allergic control group with chronic urticaria (CU; n = 29) using component-resolved diagnostics. IgE sensitization was common in both cohorts and predominantly reflected inhalant-related, cross-reactive components, particularly PR-10 proteins (63.6% in EoE vs. 37.9% in CU). In contrast, sensitization to structurally stable food allergen components, including lipid transfer proteins and plant storage proteins, was observed in a subset of patients with EoE (31.8%) and was not detected in the control group (0%; p = 0.0015). These food-derived components are characterized by resistance to thermal processing and gastrointestinal digestion and may reflect patterns of sustained dietary exposure rather than acute IgE-mediated reactions. Consistent with previous observations, component-resolved diagnostics showed limited utility for the direct identification of trigger foods in eosinophilic esophagitis. Accordingly, the observed molecular sensitization patterns should be interpreted as descriptive and hypothesis-generating signals rather than as indicators of pathogenic mechanisms or clinical decision-making tools. The findings highlight the importance of considering molecular properties of food allergen components when interpreting sensitization profiles in chronic, non-IgE-mediated inflammatory diseases and underscore the need for prospective studies integrating standardized clinical and dietary outcomes.

Eosinophilic esophagitis (EoE) is a chronic, food-driven inflammatory disorder of the esophagus in which repeated exposure to dietary antigens plays a central role, yet identification of relevant food triggers remains largely empirical. In this retrospective single-center study, molecular IgE sensitization profiles were evaluated in adult patients with EoE and compared with an allergic control group with chronic urticaria using component-resolved diagnostics. IgE sensitization was common in both cohorts and predominantly reflected inhalant-related, cross-reactive components, particularly PR-10 proteins, indicating a shared sensitization background. In contrast, sensitization to structurally stable food allergen components, including lipid transfer proteins and plant storage proteins, was observed exclusively in patients with EoE. These food-derived components are characterized by resistance to thermal processing and gastrointestinal digestion, supporting their potential relevance as markers of sustained mucosal exposure rather than acute IgE-mediated reactions. Although component-resolved diagnostics showed limited utility for direct identification of trigger foods, the selective presence of stable food ingredient sensitization may help define a distinct food-driven EoE phenotype. These findings emphasize the importance of considering molecular properties of food ingredients when interpreting sensitization patterns in chronic, diet-related inflammatory diseases. Using component-resolved diagnostics (CRD) as an immunological tool for food allergen component characterization, we highlight an emerging EoE-associated sensitization signature enriched for structurally stable, digestion-resistant allergen families. If validated prospectively, this marker pattern may support immunophenotyping and stratification of EoE patients for targeted dietary evaluation rather than stand-alone trigger identification.

Eosinophilic esophagitis (EoE) is a chronic, immune-mediated disorder characterized by eosinophilic infiltration of the esophageal epithelium, primarily driven by exposure to food and aeroallergens. Although dietary elimination remains the cornerstone of therapy, the identification of specific food triggers still largely relies on empiric methods. This narrative review explores the diagnostic and therapeutic role of component-resolved diagnostics (CRD) and other molecular tools in the personalized management of EoE. Across observational and cohort studies, CRD has shown improved sensitivity in detecting clinically relevant allergen sensitizations compared with conventional tests, allowing for more precise dietary guidance and, in some cases, reducing unnecessary food exclusions. However, remission rates achieved through CRD-guided diets remain comparable or slightly lower than those obtained with empiric elimination, highlighting the need for validation in prospective, controlled studies. Recent advances in omics-based diagnostics, including gene expression profiling and proteomic biomarkers, further underscore the potential of integrating molecular and immunologic endotyping into clinical practice. Overall, current evidence supports CRD as a promising adjunctive tool that enhances the precision of allergen identification but is not yet ready to replace empiric dietary strategies. Future research should focus on validating standardized CRD-guided algorithms, integrating omics-derived biomarkers, and developing non-invasive diagnostic platforms. Incorporating dietitian-led nutritional assessment and biomarker monitoring into CRD- and omics-informed care pathways may help prevent nutrient deficiencies, improve adherence, and translate molecular precision into safer, patient-centered dietary management.