Kefir modulates brain biomarkers and intestinal inflammation in IL-10 ^−/− mice: a novel psychobiotic perspective

<b>Background:</b> Recent studies indicate that maintaining a healthy gut microbiota balance positively influences brain function through the microbiota-gut-brain (MGB) axis. Intestinal inflammation disrupts gut microbial homeostasis, exacerbates inflammatory and oxidative processes, and reduces beneficial microbial metabolites essential for brain health. These alterations may impair MGB axis signaling and increase intestinal and blood-brain barrier (BBB) permeability, facilitating the translocation of inflammatory mediators and potentially contributing to neurological dysfunction. Kefir has emerged as a fermented food with potential psychobiotic properties due to its ability to modulate gut microbiota and its metabolites. However, its effects on brain-related outcomes during intestinal inflammation remain poorly understood.<b>Aim:</b> To investigate the association between milk kefir consumption and selected brain biomarkers in IL-10^-/^- mice.<b>Methods:</b> Male C57BL/6 mice were allocated into four groups (n = 5/group): wild-type mice receiving water (WWT), wild-type mice receiving milk kefir (KWT), IL-10^-/^- mice receiving water (WKO), and IL-10^-/^- mice receiving milk kefir (KKO). Brain analyses included cytokine levels, antioxidant activity, tight junction protein expression, and short-chain fatty acids (SCFAs), while histological evaluation focused on the small intestine.<b>Results:</b> Kefir consumption was associated with improved intestinal morphology in IL-10^-/^- mice (p < 0.03), increased brain SCFA levels (p < 0.001), reduced malondialdehyde concentrations, and higher occludin expression in brain tissue.<b>Conclusion:</b> Overall, these findings suggest that milk kefir intake may influence specific brain biomarkers in IL-10^-/^- mice. These observations provide preliminary insights and support the need for further studies to elucidate the potential psychobiotic role of kefir in intestinal inflammation.