Analysis of immune alterations and their relationship to bacterial infection after stroke

초록

Stroke blocks the blood that enters the brain, thereby inducing the death of brain cells. At the same time, stroke also causes systemic immunosuppression, resulting in secondary infections such as pneumonia or urinary infection. Thus, the interaction between brain and peripheral immune system is becoming more apparent in many researches. Therefore, we investigated to analyze the pathological phenotype of systemic immune alterations, especially T lymphocytes from early to late phase after stroke including the results of bacterial infections at the following time points: 1 and 5 days, 1 and 2 weeks, 2 and 6 months. When stroke occurred, the number of total splenocytes and thymocytes were significantly decreased in tMCAO mice at 1 week. And activated T lymphocytes were significantly increased in blood, but decreased in spleen. In addition, when lymphocytes were stimulated with α-CD3 and α-CD28 antibodies, expression of IL-2, 4, 13, and IFN-γ were decreased at 5 days. CD25 expression was also decreased in tMCAO mice. Next, we analyzed thymus. Numbers of DP (CD4+CD8+) cells were significantly decreased at 1 week after tMCAO. Development stages of thymocytes from DN1 to DN2 were also blocked. Intriguingly, the percentages of TCR-β+ cells were increased in thymocytes from tMCAO mice compared to Sham mice. Finally, we could detect bacterial infections in blood and lungs which were identified as Enterococcus faecalis, an intestinal microorganism. This infection was correlated with decreased peripheral lymphocytes numbers. Taken together, tMCAO decreased number of thymocytes and peripheral lymphocytes which may result in the increased infection of commensal bacteria.