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Stress is a biological response to threatening situations. When chronic, particularly in social contexts, it can promote behavioral, neuroinflammatory, and intestinal alterations through the gut-brain axis. Communication between the gut microbiota and the central nervous system occurs through neural, endocrine, and immune pathways. Changes in the intestinal microbiota may increase gut permeability, favoring the release of pro-inflammatory cytokines into the systemic circulation. These mediators can reach the brain, increase blood-brain barrier permeability, and contribute to neuroinflammation and behavioral changes. This study aims to investigate the influence of the gut-brain axis before and after probiotic treatment by evaluating the inflammatory profile of animals subjected to chronic social stress. In the chronic social stress model (MSA), animals underwent social regrouping at 10 weeks of age and were classified from the 12th week onward as non-regrouped (NR), harmonious (Har), defeated (AgD), or aggressors (AgR). Animals were treated with Bacillus clausii by gavage for six weeks. Intravital microscopy was performed following intravenous administration of rhodamine to evaluate cerebral leukocyte rolling and adhesion. Cytokine levels in the brain, intestine, and plasma were quantified by flow cytometry.Preliminary results from the control group showed a significant increase in IL-10 in the amygdala and IL-2 in the jejunum of AgD animals. In the prefrontal cortex, IFN-γ levels were increased in NR animals compared with AgR animals. In plasma, IL-10 levels were elevated in AgR animals, whereas IL-17A levels were increased in the NR and Har groups. Additionally, TNF-α, IFN-γ, and IL-6 levels were mainly increased in the Har and AgD groups, suggesting a systemic pro-inflammatory profile. No significant differences were observed in the hippocampus or colon, indicating the absence of a relevant inflammatory response in these regions. Cerebral leukocyte analysis revealed significantly increased leukocyte rolling and adhesion in AgD animals compared with the other groups, demonstrating enhanced cerebral inflammatory activation.These findings suggest that chronic social stress induces distinct systemic and cerebral inflammatory alterations according to behavioral phenotype, reinforcing the role of the gut-brain axis in the inflammatory response associated with chronic social stress.
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