Analysis of the Neuroinflammatory Profile of Animals Under Chronic Social Stress and Treated with Probiotics

Chronic stress, particularly when of social origin, can affect multiple physiological systems and contribute to the development of neuroinflammatory processes. Among the mechanisms involved in this response, the gut-brain axis is particularly relevant, integrating the gastrointestinal, immune, and nervous systems through bidirectional communication mediated by neural, endocrine, and immune pathways. Alterations in this axis may disrupt intestinal homeostasis and promote systemic inflammatory responses that can affect the brain environment and contribute to neuroinflammation. In this context, modulation of the gut microbiota by probiotics emerges as a potential strategy to mitigate the inflammatory effects associated with chronic stress. Thus, this study aimed to evaluate the influence of Bacillus clausii treatment on the neuroinflammatory profile in the brain of animals subjected to chronic social stress. Male mice were subjected to the Spontaneous Aggression Model (SAM), classified as non-regrouped (NR), harmonious (Har), attacked (AgD), and aggressors (AgR), and treated with B. clausii via gavage for six weeks. Neuroinflammation was assessed by intravital microscopy to analyze leukocyte rolling and adhesion and by flow cytometry to evaluate cytokine levels in different brain regions. Preliminary results from control animals showed a significant increase in IL-10 levels in the amygdala of AgD animals. In the prefrontal cortex, IFN-γ levels were increased in NR animals compared with AgR animals, whereas no significant differences were observed in the hippocampus. Analysis of cerebral leukocyte dynamics showed significantly increased leukocyte rolling and adhesion in AgD animals compared with the other groups, indicating enhanced neuroinflammatory activity in this phenotype. These results suggest that chronic social stress induces distinct neuroinflammatory responses according to behavioral phenotype. License number CEUA/IOC L-022/2025.