IL-27 regulates LPS-induced acute pneumonia in mice through STAT3 signaling pathway
WU Xia, REN Yan, WU Huimin
Public Healthcare Department, Chengdu Women’s and Children’s Central Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu 611731, China
Abstract：Objective: To investigate the role of IL-27 in lipopolysaccharide (LPS)-induced acute pneumonia in mice by regulating STAT3 signaling pathway. Methods: A total of 32 male mice were randomly divided into normal control group, LPS group, LPS+IL-27 group and LPS+IL-27 antibody group, with 8 mice in each group. After anaesthesia, the lungs of mice were taken and staining was used to observe the lung injury of mice in each group by HE. The mRNA expression levels of STAT3 and SOCS3 in lung tissue and serum of mice in each group were detected by qRT-PCR. Western blot method was used to detect the protein expression levels of STAT3, p-STAT3 and SOCS3 in lung tissue of mice in each group. The expression levels of TNF-α, IL-1β, IL-10 and TGF-β1 in lung homogenate and serum were detected by ELISA. Results: HE staining showed that in the normal control group, LPS group and LPS+IL-27 antibody group, the alveolar structure was destroyed, the alveolar wall was diffusely thickened, and there was obvious inflammatory cell infiltration. The pathological changes and inflammatory cell infiltration of LPS+IL-27 group were less than those of LPS group. Compared with the normal control group, the expression levels of STAT3 and p-STAT3 protein in lung tissue of mice in LPS group and LPS+IL-27 antibody group was significantly increased (P<0.05); the expression level of SOCS3 in LPS+IL-27 group was significantly higher than in LPS+IL-27 antibody group (P<0.05). The expression levels of TNF-α and IL-1β in lung tissue and serum of mice in each group were significantly higher than those in the normal control group (P<0.05). The expression levels of TNF-α and IL-1β in LPS+IL-27 group were significantly lower than those in LPS group and LPS+IL-27 antibody group (P<0.05). The level of IL-10 expression in LPS group and LPS+IL-27 antibody group was significantly higher than that in normal control group (P<0.05). The expression levels of IL-10 and TGF-β1 in LPS+IL-27 group was significantly higher than those in LPS+IL-27 antibody group (P<0.05). The results of immunohistochemistry showed that compared with the normal control group, TNF-α was mainly expressed in the cytoplasm of LPS group and LPS+IL-27 antibody group, while IL-1β was mainly expressed in the membrane and cytoplasm. Western blot showed that TNF-α and IL-1β were were highly expressed in lung tissue (P<0.05); the expression level of TNF-α and IL-1β in LPS+IL-27 group was significantly lower than that in LPS group and LPS+IL-27 antibody group (P<0.05). Conclusion: Exogenous IL-27 may improve LPS-induced acute pneumonia in mice by inhibiting the phosphorylation of STAT3 signaling pathway related proteins.
