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Recent studies have linked gut microorganism composition and chronic urticaria (CU); however, the underlying mechanisms responsible for this connection are unknown. Since the human immune system is in homeostasis with microbiota, and the composition of the microbiome regulates the development and function of the immune system, it is likely that an alteration of microbiota components (a dysbiosis) could influence the course of chronic spontaneous urticaria (CSU), including disease severity, patient quality of life and treatment outcome. To date, several studies have identified changes in the gut microbiota composition of patients with CSU, though only a few have exhibited metabolic abnormalities associated with gut dysbiosis. The studies on CSU patients predominantly showed that the relative abundance of beneficial bacteria was decreased (Firmicutes and Bacteroides), while that of opportunistic bacteria was increased (Enterobacteria and Proteobacteria). In addition, serum metabolome analysis revealed that gut microbiota-associated alterations in unsaturated fatty acids and the butanoate metabolism pathway may play a role in CSU. These findings are potentially associated with inflammation mediated by the imbalance of Th1/Th2/Th17 cytokines, which might contribute to CSU pathogenesis. Further research in this field could improve clinical, diagnostic, and therapeutic approaches to patients with CSU. By applying new knowledge on gut microbial communities and metabolomics, future CSU therapies could modify the microbiota composition using agents such as probiotics or other similar agents, which, in combination with current standard therapies, could hopefully lead to a reduction in symptoms and an improved quality of life for CSU patients. [ABSTRACT FROM AUTHOR]

Typical disease-associated microbiota changes are widely studied as potential diagnostic or therapeutic targets. Our aim was to analyze a hospitalized cohort including various gastroenterological pathologies in order to fine-map the gut microbiota dysbiosis. Bacterial (V3 V4) and fungal (ITS2) communities were determined in 121 hospitalized gastrointestinal patients from a single ward and compared to 162 healthy controls. Random Forest models implemented in this study indicated that the gut community structure is in most cases not sufficient to differentiate the subjects based on their underlying disease. Instead, hospitalized patients in our study formed three distinct disease non-related clusters (C1, C2, and C3), partially explained by antibiotic use. Majority of the subjects (cluster C1) closely resembled healthy controls, showing only mild signs of community disruption; most significantly decreased in this cluster were Faecalibacterium and Roseburia. The remaining two clusters (C2 and C3) were characterized by severe signs of dysbiosis; cluster C2 was associated with an increase in Enterobacteriaceae and cluster C3 by an increase in Enterococcus. According to the cluster affiliation, subjects also showed different degrees of inflammation, most prominent was the positive correlation between levels of C-reactive protein and the abundance of Enterococcus. [ABSTRACT FROM AUTHOR]