ArticlePhysiological reports2026
IL-17RA/RC blockade modulates the fibrinolytic system and MMP activity in bleomycin-induced pulmonary fibrosis in male mice.
Article in Physiological reports, 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
Idiopathic pulmonary fibrosis (IPF) is a fatal interstitial lung disease with excessive accumulation of extracellular matrix (ECM) components, which leads to disrupted lung architecture and respiratory failure. Interleukin (IL)-17 signaling induces fibrosis through inflammation; however, specific roles of its receptors IL-1RA and IL-17RC in fibrinolysis and ECM remodeling remain unclear. We hypothesized that inhibition of either IL-17RA or IL-17RC could reduce fibrosis by regulating MMP expression and function. In this study, a Bleomycin (BLM)-induced murine model of pulmonary fibrosis was used to study the effect of neutralization of IL-17RA and IL-17RC on ECM remodeling, MMPs, and the fibrinolytic system. Fibrotic lungs showed increased levels of MMP-2 and MMP-9, corresponding with elevated expression of fibronectin and collagen. Neutralization of either IL-17RA or IL-17RC significantly reduced the expression of MMPs, activation of NF-κB, and restored normal fibrinolytic activity by upregulating uPA and downregulating PAI-1 levels.
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