IL-22 alleviates sepsis-induced acute lung injury by inhibiting epithelial cell apoptosis via STAT3 signalling

Abstract Background Sepsis is a critical condition in which organ dysfunction occurs because of aberrant response to infection, resulting in a life-threatening situation. The lung, which is the most vulnerable target organ, often experiences severe damage. IL-22, which is secreted by various immunocytes, can mitigate inflammation associated with pulmonary fibrosis and lung injury. Nevertheless, its precise function in SALI is still unclear. The current investigation was undertaken to delve into the effect of IL-22 in sepsis. Methods: In this study, a mouse CLP model of sepsis was used to detect the expression of IL-22 and investigate the effect of rIL-22 treatment, following which the survival rate and lung tissue injury and apoptosis was determined. LPS induced bronchial epithelial cells ( BEAS-2B) apoptosis model with or without rIL-22 in vitro to further evaluate the effect and mechanism of IL-22. Results The level of IL-22 in serum and lung tissue was increased after CLP. rIL-22 administration increased the survival rates of septic mice and suppressed the secretion of proinflammatory cytokines, and alleviated SALI. IL-22 also alleviated apoptosis in lung tissue and decreased the level of cleaved caspase-3/7.Furthermore, rIL-22 alleviated LPS induced BEAS-2Bs apoptosis which was associated with an increase in the phosphorylation of STAT3. Conclusions The results of this study suggest that IL-22 alleviates lung epithelial cell apoptosis and protects mice against SALI via the STAT3 signalling pathway,emphasizing its potential therapeutic value for sepsis.