Alopecia areata (AA) is a complex autoimmune disorder with multifactorial pathogenesis. Recent research highlights the gut microbiota as a possible key player in AA pathogenesis through the gut–skin axis: gut dysbiosis may disrupt intestinal barrier integrity and immune tolerance by affecting T regulatory cells, potentially contributing to disease onset and progression. The purpose of this review is to analyze the current evidence on the correlation between gut microbiota and AA, dissecting both the pathogenetic role of its alterations in the onset and progression of disease and its potential role as a therapeutic target.

Background: Untargeted microbiome modulation has achieved conflicting results in post-infectious irritable bowel syndrome (PI-IBS). Methods: In a case–control study of PI-IBS patients, cases received targeted microbial modulation informed by microbiome profiling, while controls were managed by standard therapy. Treatment response was defined as a decrease in IBS-symptom severity scale (IBS-SSS) ≥50 points. Results: All thirteen cases (100%) and 11/20 controls (55%) experienced treatment response (p < 0.0001). The mean IBS-SSS score after treatments was 163 in cases and 231 in controls (p = 0.01). Conclusions: Based on our preliminary results, therapeutic microbiome modulation might be a promising strategy for PI-IBS. Further studies are needed to clarify its role.

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Proton pump inhibitors (PPIs) are among the most widely used drugs in clinical practice. Although generally effective and well tolerated, their widespread and frequently prolonged use has raised concerns about both gastrointestinal and systemic adverse effects. Some of these effects may be directly or indirectly mediated by proton-pump-inhibitor-induced alterations of the gut microbiota. Proton pump inhibitors can reshape gastrointestinal microbial communities through multiple mechanisms, including gastric acid suppression, impaired barrier function, and modulation of the immune and metabolic pathways. The resulting dysbiosis promotes oral-to-gut microbial translocation, reduces microbial diversity, and favors the expansion of potentially pathogenic taxa. These alterations have been associated with several gastrointestinal disorders such as small intestinal bacterial overgrowth, enteric infections, and disturbances of the gut–liver axis, while emerging evidence suggests broader implications for carcinogenesis and the response to immune checkpoint inhibitors. In this context, microbiota-modulating interventions, including probiotics, may provide clinical benefits; however, the current evidence remains limited and inconsistent, precluding their routine use. By integrating mechanistic and clinical evidence, this review aims to clarify the role of the gut microbiota in proton-pump-inhibitor-related adverse effects and to assess the potential of microbiota-targeted strategies to mitigate their clinical consequences.

Proteobacteria are a phylum of Gram-negative bacteria that, although normally a minor component of the healthy gut microbiota, can be markedly increased in many conditions. Their overgrowth is in fact linked to inflammation, impaired epithelial barrier function, and diseases such as inflammatory bowel disease, metabolic syndrome, and gastrointestinal cancers. Key species, like Escherichia coli and Helicobacter pylori, can promote disease through specific etiopathogenetic mechanisms, from genotoxin production to immune activation: this peculiarity can be used for diagnostic purposes, and in some cases even as therapeutics. Emerging microbiota-targeted therapies—such as dietary modulation, probiotics, fecal microbiota transplantation, bacteriophages, and engineered bacteria—aim to restore microbial balance. This narrative review deals with the dual role of Proteobacteria as both pathogens and diagnostic–therapeutic tools, which is crucial for advancing personalized microbiome-based medicine.

Tryptophan (Trp) metabolism lies at the intersection of nutrition, gut microbiota, mucosal immunology, and systemic inflammation—processes that play key roles in many gastrointestinal and extraintestinal diseases. Trp is an essential amino acid obtained through dietary intake. Beyond its role in protein synthesis, it is metabolized through three principal pathways: the kynurenine pathway, the serotonin/melatonin pathway, and microbial metabolism in the gut leading to indole and related derivatives. The kynurenine pathway represents the primary route of Trp degradation and is strongly linked to inflammatory signaling. The serotonin pathway is particularly important for gastrointestinal physiology, influencing motility, secretion, and visceral sensitivity. In parallel, microbial Trp metabolism produces metabolites that regulate epithelial barrier integrity, modulate mucosal immune responses, and contribute to communication along the gut–organ axes. Across different disease states, several recurring patterns emerge. Inflammatory conditions frequently shift Trp metabolism toward the kynurenine pathway through increased IDO1 or TDO activity, resulting in changes in kynurenine metabolites and in the kynurenine-to-tryptophan (Kyn/Trp) ratio. At the same time, reduced microbial production of indole derivatives may impair aryl hydrocarbon receptor signaling and weaken barrier-protective and immunoregulatory mechanisms. Alterations in the serotonin pathway are also associated with disturbances in gastrointestinal motility and gut–brain communication. Together, these observations highlight Trp metabolism as an important framework for understanding interactions between diet, microbiota, and host responses in health and disease. However, it is important to clarify that much of the currently available evidence remains associative or is derived primarily from preclinical models. This narrative review, based on literature retrieved from major biomedical databases (e.g., PubMed/MEDLINE, Scopus, and Web of Science), aims to provide an updated synthesis of current knowledge on Trp metabolism in disease pathophysiology. Furthermore, while we highlight potential translational applications—such as proposed biomarker development and targeted therapeutic strategies—these perspectives have been moderated to acknowledge the limited level of clinical validation established to date.