ArticleFrontiers in immunology2026
Early CCR2-dependent monocyte recruitment defines a critical neuroinflammatory window after subarachnoid hemorrhage.
Article in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Subarachnoid hemorrhage (SAH) remains a devastating cerebrovascular disease with limited therapies targeting secondary neurological injury. Increasing evidence suggests that the early brain injury (EBI) period within the first 72h after SAH represents a critical therapeutic window characterized by diffuse neurovascular and inflammatory activation within the cerebrospinal fluid (CSF) and meningeal compartments. Although resident microglial responses during EBI have been extensively investigated, the contribution of infiltrating CCR2-dependent monocytes to inflammatory amplification and secondary neuronal injury during this acute phase remains incompletely defined. Here, we investigated the temporal role of CCR2-dependent monocyte recruitment during EBI following experimental SAH. Using a murine endovascular perforation model, we evaluated outcomes in CCR2-deficient mice and wild-type mice treated with a pharmacologic CCR2 antagonist at distinct post-SAH timepoints. CCR2 deletion or early pharmacologic inhibition significantly reduced Ly6C
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