Interleukin-17A promotes paraquat-induced acute lung injury on mice

Objective: Interleukin-17A (IL-17A) is a potent proinflammatory factor. Our study aimed to investigate the role of IL-17A on acute lung injury (ALI) induced by paraquat (PQ) and the potential way. Methods: A total of 180 female mice were randomly and evenly divided into 9 groups: Control group (NS), PQ groups (4 groups) and PQ+A b groups (4 groups). NS group mice were treated with equal volume of physiological saline by gastric gavage. Mice in PQ and PQ+A b groups were exposed to PQ solution by gastric gavage (25 mg/kg). PQ+A b groups mice were intraperitoneally (i.p.) injected with IL-17A neutralizing antibody (5 mg/kg) 2 hours after PQ perfusion, all of managements above were one-off. Mice were executed respectively at 8 h, 24 h, 48 h and 72 h, NS group mice at 24 h. Lung pathological change was observed with HE staining, wet-to-dry (W/D) ratio and total protein content in broncho-alveolar lavage fluid (BALF) were determined, changes of cytokines were detected by ELISA, leukocyte and neutrophil in BALF were recorded, lung IL-17A and Nuclear Factor-κB p65 (NF-κB p65) were examined by immunohistochemical (IHC), q-PCR was used for the expression of IL-17A mRNA in lung tissue. Results: After PQ perfusion, levels and expression of IL-17A in mice increased (P<0.05); While blockade IL-17A with antibody, the ALI induced by PQ was attenuated, activation of NF-κB p65 and the percentage of neutrophil were reduced (P<0.05). Conclusion: IL-17A promotes the process of ALI induced by PQ, and probably by activating NF-κB p65 and recruiting neutrophil.