Post-stroke inflammation

Post-stroke inflammation represents the cascade of immune and inflammatory processes triggered after brain tissue injury following ischemic or hemorrhagic stroke. It begins with the release of damage-associated molecular patterns (DAMPs) from injured neurons, which are sensed by pattern recognition receptors (PRRs) such as Toll-like receptors (TLRs), NOD-like receptors (NLRs), and C-type lectin receptors (CLRs) on microglia and infiltrating immune cells. This activation results in the secretion of pro- and anti-inflammatory cytokines (including TNF-α, interleukins such as IL-1β, IL-6, IL-10), chemokines (e.g., MCP-1), and other mediators. While early inflammation often contributes to infarct expansion and neuronal death (by promoting edema, blood-brain barrier breakdown, and leukocyte infiltration), later phases of inflammation assist in clearing debris and supporting tissue repair and remodeling. Thus, inflammation post-stroke has both detrimental and beneficial roles depending on timing and context. Multiple drugs can target specific pro-inflammatory mediators (e.g., anti-TNF, IL-1 blockers) for potential neuroprotection, but directly targeting "post-stroke inflammation" as a single entity is not feasible and carries therapeutic challenges due to the complexity and dual nature of inflammatory responses.

Other names

Poststroke inflammationPost-stroke neuroinflammationStroke-induced inflammation