The Gut-Brain-Immune Axis: Role of Microbiota Dysbiosis and Autonomic Nervous System in Infectious Diseases

The human gastrointestinal tract harbors a complex microbial ecosystem that plays a fundamental role in maintaining immune balance and defending against infectious diseases. Disruption of this ecosystem, known as dysbiosis, has been increasingly associated with impaired immune responses and heightened susceptibility to infections. Emerging evidence highlights the importance of the gut-brain-immune axis, particularly the role of the autonomic nervous system (ANS), in regulating these interactions. This systematic review aimed to examine the relationship between gut microbiota dysbiosis and infectious diseases, with specific emphasis on the influence of autonomic dysfunction on disease susceptibility and outcomes. A comprehensive search of PubMed/Medical Literature Analysis and Retrieval System Online (MEDLINE), Scopus, and Google Scholar was conducted to identify relevant observational studies published between 2000 and 2025. Data extraction and quality assessment were performed using standardized tools, including the Newcastle-Ottawa Scale (NOS). A total of 11 studies were included in the qualitative synthesis. The included studies consistently demonstrated that dysbiosis is associated with reduced microbial diversity and loss of beneficial taxa, which in turn were linked to increased infection risk and disease severity. Additionally, autonomic imbalance, reflected by increased sympathetic activity and reduced parasympathetic (vagal) tone, was frequently associated with impaired immune regulation. Reduced heart rate variability was commonly reported, suggesting a potential link between microbial alterations and neuroimmune dysfunction. Overall, the findings suggest that gut microbiota dysbiosis may be associated with infectious disease outcomes, with ANS dysfunction acting as a potential modulatory pathway. These findings should be interpreted with caution, as the included studies are predominantly observational and mechanistic. The results are therefore hypothesis-generating rather than practice-changing, and further high-quality studies are required to establish causal relationships.