Frontiers in immunology · 2026
IL-17A-associated PTGS2 and MMP9 inflammatory signaling in ischemic stroke: clinical correlation and experimental evidence.
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Hou Chunlan, Yang Zilong, Wang Baoai
Аннотация
BACKGROUND: 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.
METHODS: 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.
RESULTS: 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 < 0.001). IL-17A was positively correlated with PTGS2 (rho = 0.292, P < 0.01), MMP9 (rho = 0.216, P < 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.
CONCLUSION: 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.
METHODS: 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.
RESULTS: 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 < 0.001). IL-17A was positively correlated with PTGS2 (rho = 0.292, P < 0.01), MMP9 (rho = 0.216, P < 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.
CONCLUSION: 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.