The impact of acute inflammation on the brain immune environment 2896

Abstract Description Neuroinflammation is typically attributed to the sustained activation of resident immune cells in the brain, such as microglia. However, in acute inflammation, cells are activated rapidly and reconstruct the blood-brain barrier (BBB) in order to prevent further damage. Given that acute inflammation causes significant damage to the brain in a short period of time, the impact on the immune system may persist for an extended duration. In this study, we observed a significant infiltration of monocytes and macrophages into the brain following the induction of acute inflammation by LPS. This infiltration was accompanied by a reduction in IL-10 and an increase in IL-1β levels one day after injection, which then returned to baseline within a week. The number of microglia decreased transiently; however the cytokine expression pattern was comparable to that of macrophages. Notably, despite restoring motor and memory functions in mice, the microglial phenotype remained unresponsive even after one month. Also, those microglia exhibited numerous similarities with the chronic Alzheimer’s model at the gene level. Furthermore, acute inflammation induced by LCMV also results in temporal BBB impairment and persistent microglial phenotype alteration. In conclusion, our findings verified that acute inflammation affects the immune microenvironments of the brain in a long-lasting way, suggesting that severe inflammation may increase the risk of developing neurodegenerative disease in the future. Topic Categories Neuroimmunology (NEUR)