β2-Integrins Regulate Microglial Responses and the Functional Outcome of Hemorrhagic Stroke In Vivo

Stroke is one of the leading causes of death and long-term disabilities worldwide. In addition to interruption of blood flow, inflammation is widely recognized as an important factor mediating tissue destruction in stroke. Depending on their phenotype, microglia, the main leukocytes in the CNS, are capable of either causing further tissue damage or promoting brain restoration after stroke. β2-integrins are cell adhesion molecules that are constitutively expressed on microglia. The function of β2-integrins has been investigated extensively in animal models of ischemic stroke, but their role in hemorrhagic stroke is currently poorly understood. We show in this study that dysfunction of β2-integrins is associated with improved functional outcome and decreased inflammatory cytokine expression in the brain in a mouse model of hemorrhagic stroke. Furthermore, β2-integrins affect microglial phenotype and cytokine responses in vivo. Therefore, our findings suggest that targeting β2-integrins in hemorrhagic stroke may be beneficial.