The Effect of Microbiota and Evaluation of Released Cytokines in Schizophrenia Patients

Bidirectional communication between the gut microbiota and the brain has been increasingly recognized, with growing evidence suggesting its relevance in schizophrenia. Altered microbiota composition may contribute to gastrointestinal barrier disruption, immune activation, and metabolic dysfunction. Given the multifactorial etiology of schizophrenia involving genetic, epigenetic, and environmental factors, microbiota-related mechanisms may represent an important pathway in disease development. This prospective, controlled study investigated gut microbiota composition and systemic inflammatory markers in schizophrenia patients. Blood and stool samples were obtained from 14 patients with schizophrenia and 6 matched healthy controls. Microbiota profiles were determined through 16 S rRNA gene sequencing, while serum levels of Claudin-1, Occludin, E-cadherin, Zonulin, IL-1β, IL-6, and TNF-α were analyzed using ELISA. Firmicutes and Bacteroidota were the predominant phyla in both groups. However, alpha diversity (Shannon index, p < 0.05) and beta diversity (Permanova, p < 0.01) analyses showed significant differences between patients and controls. ELISA results demonstrated significantly elevated levels of IL-1β, IL-6, TNF-α, Claudin-1, and E-cadherin (all p < 0.05) in patients, whereas Occludin was significantly decreased (p < 0.05) and Zonulin levels were unexpectedly lower compared to controls. Results indicate significant gut dysbiosis and heightened systemic inflammation in schizophrenia patients. This interplay between microbial composition, intestinal permeability, and inflammatory processes may contribute to the pathophysiology of the disorder. Further studies with larger cohorts, including antipsychotic-naïve first-episode patients, are warranted to clarify causality and evaluate microbiota-targeted interventions as potential therapeutic strategies.