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

ABSTRACT: 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 ?1 chain (COL1?1) and collagen type I ?2 chain (COL1?2). 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 COL1?1 and COL1?2 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.

SUBMITTER: Liu J

PROVIDER: S-EPMC7401847 | biostudies-literature | 2020 Sep

REPOSITORIES: biostudies-literature

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

Liu Juan J Shang Biao B Bai Jing J

Experimental and therapeutic medicine 20200624 3

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 ...[more]

PMID: 32765690

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Project description:BACKGROUND:Serum IL-22 levels are increased in patients with atopic dermatitis, which commonly precedes asthma in the atopic march. Epicutaneous sensitization in mice results in TH2-dominated skin inflammation that mimics atopic dermatitis and sensitizes the airways for antigen challenge-induced allergic inflammation characterized by the presence of both eosinophils and neutrophils. Epicutaneous sensitization results in increased serum levels of IL-22. OBJECTIVE:We sought to determine the role of IL-22 in antigen-driven airway allergic inflammation after inhalation challenge in epicutaneously sensitized mice. METHODS:Wild-type (WT) and Il22-/- mice were sensitized epicutaneously or immunized intraperitoneally with ovalbumin (OVA) and challenged intranasally with antigen. OVA T-cell receptor-specific T cells were TH22 polarized in vitro. Airway inflammation, mRNA levels in the lungs, and airway hyperresponsiveness (AHR) were examined. RESULTS:Epicutaneous sensitization preferentially elicited an IL-22 response compared with intraperitoneal immunization. Intranasal challenge of mice epicutaneously sensitized with OVA elicited in the lungs Il22 mRNA expression, IL-22 production, and accumulation of CD3+CD4+IL-22+ T cells that coexpressed IL-17A and TNF-?. Epicutaneously sensitized Il22-/- mice exhibited diminished eosinophil and neutrophil airway infiltration and decreased AHR after intranasal OVA challenge. Production of IL-13, IL-17A, and TNF-? was normal, but IFN-? production was increased in lung cells from airway-challenged and epicutaneously sensitized Il22-/- mice. Intranasal instillation of IFN-?-neutralizing antibody partially reversed the defect in eosinophil recruitment. WT recipients of TH22-polarized WT, but not IL-22-deficient, T-cell receptor OVA-specific T cells, which secrete both IL-17A and TNF-?, had neutrophil-dominated airway inflammation and AHR on intranasal OVA challenge. Intranasal instillation of IL-22 with TNF-?, but not IL-17A, elicited neutrophil-dominated airway inflammation and AHR in WT mice, suggesting that loss of IL-22 synergy with TNF-? contributed to defective recruitment of neutrophils into the airways of Il22-/- mice. TNF-?, but not IL-22, blockade at the time of antigen inhalation challenge inhibited airway inflammation in epicutaneously sensitized mice. CONCLUSION:Epicutaneous sensitization promotes generation of antigen-specific IL-22-producing T cells that promote airway inflammation and AHR after antigen challenge, suggesting that IL-22 plays an important role in the atopic march.

Dataset Information

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

Publications

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

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