{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,1]],"date-time":"2026-07-01T08:34:29Z","timestamp":1782894869168,"version":"3.54.5"},"reference-count":33,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,7,1]],"date-time":"2026-07-01T00:00:00Z","timestamp":1782864000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Immunol."],"abstract":"<jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>IL-17A is implicated in post-stroke inflammation, but its downstream inflammatory mediators in ischemic stroke remain incompletely defined. This study investigated whether IL-17A-associated signaling is linked to PTGS2 and MMP9 expression in ischemic stroke and whether IL-17A neutralization modulates these changes after cerebral ischemia.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>Three GEO datasets were analyzed to identify candidate genes and enriched pathways. Serum IL-17A, PTGS2, and MMP9 levels were measured by ELISA in patients with acute ischemic stroke and controls, and their associations with admission National Institutes of Health Stroke Scale (NIHSS) scores were examined. A rat middle cerebral artery occlusion (MCAO) model was established, and IL-17A neutralizing antibody treatment was used to assess effects on inflammatory markers, neurological deficits, and infarct volume.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>Bioinformatics analysis prioritized PTGS2 and MMP9 as candidate inflammatory genes enriched in the IL-17 signaling pathway. Serum IL-17A, PTGS2, and MMP9 levels were significantly elevated in patients with ischemic stroke versus controls (all P &amp;lt; 0.001). IL-17A was positively correlated with PTGS2 (rho = 0.292, P &amp;lt; 0.01), MMP9 (rho = 0.216, P &amp;lt; 0.05), and admission NIHSS score. In MCAO rats, IL-17A, PTGS2, and MMP9 expression increased together with PGE2 and IL-6 levels. IL-17A neutralizing antibody treatment was associated with reduced PTGS2 and MMP9 expression, lower PGE2 and IL-6 levels, decreased infarct volume, and improved neurological deficit scores in MCAO rats, although an isotype-matched IgG control was not included.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>These findings support an IL-17A-associated PTGS2\/MMP9 inflammatory network in ischemic stroke and suggest that IL-17A-associated inflammatory signaling may represent a biologically relevant pathway in post-ischemic injury, warranting further validation in studies incorporating appropriate isotype-matched antibody controls.<\/jats:p>\n                  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