Expression of IL-17A and IL-17F in lipopolysaccharide-induced acute lung injury and the counteraction of anisodamine or methylprednisolone.

Th17 cytokines IL-17A and IL-17F as pro-inflammatory cytokines played an important role in triggering inflammatory responses. However, little was known about the expression of IL-17A and IL-17F in acute lung injury (ALI). Therefore, the present study investigated the expression of IL-17A and IL-17F in lipopolysaccharide (LPS)-induced ALI in rats and rat pulmonary microvascular endothelial cells (PMVEC) by enzyme-linked immunosorbant assay or reverse transcription-polymerase chains reaction. Anisodamine and methylprednisolone were also investigated as anti-inflammatory strategy in the process of LPS-induced ALI. Lung injury was evaluated by histological changes, right lung wet weight:body weight (LW/BW) ratios, and protein education and total leukocyte count of bronchoalveolar lavage fluid (BALF). Our findings showed that LPS exposure elevated the levels of leukocyte number, protein education in BALF and the ratios of LW/BW, increased the expression of IL-17A and IL-17F in the lung tissues homogenate, BALF and serum of ALI rats. Up-regulation of IL-17F expression was also observed after LPS challenge in rat PMVEC. Treatment with anisodamine or methylprednisolone significantly inhibited the increases of parameters of ALI induced by LPS, and markedly reduced the expression of IL-17A and IL-17F in rats and the IL-17F expression in PMVEC. These data suggested that IL-17A and IL-17F maybe play an important role in LPS-induced ALI via autocrine and paracrine mechanisms, and anisodamine is similar in extent to methylprednisolone that contributes to relieve LPS-induced ALI.