IL-22/IL-22R1 promotes proliferation and collagen synthesis of MRC-5 cells via the JAK/STAT3 signaling pathway and regulates airway subepithelial fibrosis

Asthma in children poses a threat to their health, but the mechanism remains to be elucidated. The present study investigated the mechanism by which the interleukin (IL)-22/IL-22 Receptor 1 (IL-22R1) signaling pathway regulates subepithelial fibrosis in children with asthma. A total of 41 children with asthma and 12 healthy children were included in the present study. ELISA was performed to measure the content of IL-22 in peripheral blood. Serum from children with asthma was used to incubate MRC-5 cells and IL-22 antibody rescued the effect of IL-22 on the biological functions of MRC-5 cells. Reverse transcription-quantitative PCR was performed to determine IL-22R1 mRNA expression levels and western blotting was performed to measure IL-22R1 protein expression. The Cell Counting Kit-8 assay was used to analyze cell proliferation and flow cytometry was performed to assess the cell cycle distribution of MRC-5 cells. The expression of IL-22 was elevated in peripheral blood from children with asthma, which promoted the proliferation of MRC-5 cells, possibly via the upregulation of collagen type I α1 chain (COL1α1) and collagen type I α2 chain (COL1α2). IL-22 exerted its biological functions via IL-22R1. The IL-22/IL-22R1 signaling pathway regulated the proliferation of MRC-5 cells and the expression of COL1α1 and COL1α2 in MRC-5 cells via the JAK/STAT3 signaling pathway. Mononuclear lymphocytes from children with asthma stimulated the proliferation and secretory function of fibroblasts by secreting IL-22. The present study suggested that IL-22 expression in peripheral blood of children with asthma is upregulated compared with the control group. Furthermore, the present study indicated that the IL-22/IL-22R1 signaling pathway promoted MRC-5 cell proliferation and collagen synthesis by activating the JAK/STAT3 signaling pathway, thereby potentially regulating airway subepithelial fibrosis.