Molecular and cellular mechanisms underlying the sterile inflammation after ischemic stroke

Abstract

Inflammation is an essential step for the pathology of ischemic stroke, and is also an important therapeutic target for developing novel therapeutic methods which have a wide therapeutic time window. Since there is no pathogen in the brain, the inflammation will be triggered by some endogenous molecules which are called as danger associated molecular patterns (DAMPs). So far two important DAMPs, high mobility group box 1 (HMGB1) and peroxiredoxin (PRX), have been recently identified in the ischemic brain. HMGB1 exaggerates the disruption of blood brain barrier; on the other hand, PRX activates mononuclear phagocytes and induces the inflammatory cytokine production through the activation of Toll-like receptor 2 (TLR2) and TLR4. Various inflammatory molecules produced from infiltrating immune cells have been known to exacerbate the neurological deficits of ischemic stroke patients. Recently, it has been paid attention that the inflammation after tissue injury also induces tissue repair, while its mechanisms remain to be clarified. Novel therapeutic methods will be established by clarifying detailed molecular mechanisms underlying the induction of neural repair after cerebral post-ischemic inflammation.