Acute lung injury caused byCandida albicans could result in high mortality and morbidity. MicroRNA-155 (miR-155) and suppressor of cytokine signaling 1 (SOCS1) have been believed to play a key in the regulation of inflammatory response. Whether miR-155/SOCS1 axis could regulate the acute lung injury caused by C. albicans has not been reported. The acute lung injury animal model was established with acute infection of C. albicans. miR-155 inhibitor, miR-155 mimic, and sh-SOCS1 were constructed. The binding site between miR-155 and SOCS1 was identified with dual luciferase reporter assay. Knockdown of miR-155 markedly inhibited the germ tube formation of C. albicans. Knockdown of miR-155 significantly up-regulated the expression of SOCS1, and the binding site between miR-155 and SOCS1 was identified. Knockdown of miR-155 improved the acute lung injury, suppressed inflammatory factors and fungus loading through SOCS1. Knockdown of SOCS1 greatly reversed the influence of miR-155 inhibitor on the cell apoptosis in vitro. The improvement of acute lung injury caused by C. albicans, suppression of inflammatory response and C. albicans infection, and inhibitor of cell apoptosis were achieved by knocking down miR-155 through SOCS1. This research might provide a new thought for the prevention and treatment of acute lung injury caused by C. albicans through targeting miR-155/SOCS1 axis.

Objectives To address the effect and mechanism of Monotropein (Mon) on sepsis-induced acute lung injury (ALI). Methods ALI model was established by lipopolysaccharide (LPS)-stimulated mouse lung epithelial cell lines (MLE-12) and cecal ligation and puncture (CLP)-treated mice, respectively. The function of Mon was examined by cell counting kit-8 (CCK-8), pathological staining, the pulmonary function examination, flow cytometry, enzyme-linked immunosorbent assay, terminal deoxynucleotidyl transferase deoxyuridine triphosphate nick end labellingand western blot. Results Mon increased the LPS-reduced viability but decreased the LPS-evoked apoptosis rate in MLE-12 cells. Mon suppressed the concentrations and protein expressions of proinflammatory factors, and the expressions of fibrosis-related proteins in LPS-challenged MLE-12 cells compared with LPS treatment alone. Mechanically, Mon downregulated the levels of NF-κB pathway, which was confirmed with the application of the receptor activator of nuclear factor-κB ligand (RANKL). Correspondingly, RANKL reversed the ameliorative effect of Mon on the proliferation, apoptosis, inflammation and fibrosis. Moreover, Mon improved the pathological manifestations, apoptosis, the W/D ratio and pulmonary function indicators in CLP-treated mice. Consistently, Mon attenuated inflammation, fibrosis and NF-κB pathway in CLP-treated mice. Conclusion Mon inhibited apoptosis, inflammation and fibrosis to alleviate sepsis-evoked ALI via the NF-κB pathway.