Abstract
Interleukin-17A (IL-17A) is involved in multiple inflammatory diseases. Our study was to investigate the role of IL-17A on acute lung injury (ALI) respectively induced by lipopolysaccharide (LPS) and paraquat (PQ) on mice. We built ALI mouse models respectively by single intraperitoneal (i.p.) injection with LPS or single gavage with PQ liquid. Two hours after the models were established, a dosage of neutralizing antibody was used to blockade IL-17A by i.p. injection. At 8, 24, and 48 h, the lung wet-to-dry ratio (W/D) was calculated and total protein in bronchoalveolar lavage fluid (BALF) was measured; hematoxylin-eosin staining was used to observe lung tissue pathological changes; inflammatory cells in BALF were recorded with a hemocytometer; cytokines were measured with enzyme-linked immunosorbent assay kits; immunohistochemistry examined the expression of IL-17A and activation of nuclear factor-κB p65 (NF-κB p65); and qPCR determined the expression of IL-17A mRNA. After being administered with LPS or PQ, all mice presented ALI pathological change; expression of IL-17A increased significantly. When blocking IL-17A with antibody, lung injury in both LPS- and PQ-administrated mice was attenuated. All the above tests decreased. Compared with those in PQ mice, IL-17A levels in LPS mice were higher. IL-17A involves the ALI induced by LPS or PQ and promotes the pathological process by activating NF-κB P65 and recruiting neutrophils, which enlarges the cascade effect of inflammation and injures lung tissues. And when blockading IL-17A with antibody, the ALI is alleviated. The reaction of IL-17A in the ALI induced by LPS is stronger than that by PQ.