Related Experiment Video
Updated: Jul 17, 2026
Isolation and Flow Cytometric Assessment of Neuroimmune Interactions in a Mini-Stroke Murine Model
Published on: June 20, 2025
IL-17A-associated PTGS2 and MMP9 inflammatory signaling in ischemic stroke: clinical correlation and experimental
Chunlan Hou1,2, Zilong Yang1,2, Baoai Wang1,2
1Graduate School, Shanxi Medical University, Taiyuan, Shanxi, China.
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.
Insights
Interleukin-17A (IL-17A) drives inflammation in ischemic stroke by increasing PTGS2 and MMP9. Neutralizing IL-17A reduced stroke-related inflammation, infarct volume, and improved neurological deficits in a rat model.
Area of Science:
- Neuroscience
- Immunology
- Biochemistry
Background:
- Interleukin-17A (IL-17A) plays a role in post-stroke inflammation.
- Downstream inflammatory mediators of IL-17A in ischemic stroke are not fully understood.
Purpose of the Study:
- To investigate the link between IL-17A signaling and the expression of PTGS2 and MMP9 in ischemic stroke.
- To determine if IL-17A neutralization can modulate these inflammatory changes after cerebral ischemia.
Main Methods:
- Bioinformatic analysis of GEO datasets to identify candidate genes and pathways.
- Measurement of serum IL-17A, PTGS2, and MMP9 levels in ischemic stroke patients and controls.
- Assessment of IL-17A neutralization effects in a rat middle cerebral artery occlusion (MCAO) model.
Main Results:
- PTGS2 and MMP9 were identified as candidate inflammatory genes within the IL-17 signaling pathway.
- Serum levels of IL-17A, PTGS2, and MMP9 were significantly elevated in stroke patients.
- IL-17A neutralization in MCAO rats reduced PTGS2/MMP9 expression, infarct volume, and improved neurological deficits.
Conclusions:
- Findings support an IL-17A-associated PTGS2/MMP9 inflammatory network in ischemic stroke.
- IL-17A signaling represents a potential therapeutic target for post-ischemic injury.
Related Concept Videos
01:15Ischemic Stroke ll: Pathophysiology
01:29Hemorrhagic Stroke ll: Pathophysiology