Responses of Immune Organs after Cerebral Ischemic Stroke.

Abstract

BACKGROUND: Stroke is a leading cause of death and disability worldwide. Recently, secondary damage to the brain has been hypothesized as a key aggravating element in the ischemic cascade. However, the interaction between cerebral infarction and immune organs is not fully understood. In this study, we investigated changes in rat brain, spleen, thymus, mesenteric lymph node, and liver at 3, 7, and 13 days after transient middle cerebral artery occlusion (tMCAO) by immunohistochemistry. METHODS: Rat models of stroke were made by tMCAO. Functional assessment was performed at 3 h and 1, 3, 5, 7, 9, 11, and 13 days after MCAO. Rat organs were harvested for 2,3,5-triphenyltetrazolium chloride staining and immunohistochemistry. RESULTS: The number of CD8αT cells decreased in spleen, thymus, mesenteric lymph node, and liver and increased in brain. Numbers of Iba1and CD68macrophages decreased in spleen, thymus, and mesenteric lymph node and increased in brain and liver. Ki67cells exhibited the same characteristics as macrophages, and increased numbers of terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end labeling (TUNEL) -positive apoptotic cells were present in spleen, mesenteric lymph node, liver, and brain. CONCLUSIONS: The present results indicate that stroke is a systemic disease that, in addition to affecting the brain, also induces responses in immune organs. These results suggest that systemic treatment might be a good strategy for clinical stroke care.