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. CCL9 antibody and RNA interference approaches were used to interrogate the signalling pathway. Following cerebral I/R, microglial activation led to increased ROS production, and increased SPI1 and CCL9 expression. This, in turn, increased CCL9 secretion, which attracted macrophages to the site of ischemia and promoted their polarization towards a pro‑inflammatory phenotype. Inhibition of the ROS‑SPI1‑CCL9 axis significantly reduced macrophage infiltration and altered their polarization state. The results of the present study demonstrated that microglia facilitated macrophage infiltration and polarization in cerebral I/R via the ROS‑SPI1‑CCL9 axis, highlighting a potential therapeutic target for mitigating neuroinflammatory damage after a cerebral ischemic stroke.
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Kuang et al. (2026) studied this question.
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