TY - EJOU
AU - Huang, Chuanjun
AU - Sun, Yan
AU - Liu, Na
AU - Zhang, Ziping
AU - Wang, Xiyan
AU - Lu, Degan
AU - Zhou, Ling
AU - Zhang, Caiqing
TI - IL-27 attenuates airway inflammation and epithelialmesenchymal transition in allergic asthmatic mice possibly via the RhoA/ROCK signalling pathway
T2 - European Cytokine Network
PY - 2022
VL - 33
IS - 1
SN - 1952-4005
AB - Background: Asthma is an airway disease characterized by airflow limitation and various additional clinical manifestations. Repeated inflammatory stimulation of the airways leads to epithelial-mesenchymal transition (EMT) which aggravates subepithelial fibrosis during the process of airway remodelling and enhances resistance to corticosteroids and bronchodilators in refractory asthma. There is growing evidence that IL-27 modulates airway remodelling, however, the molecular mechanisms involving IL-27 and EMT are poorly understood. The objective of this study was to investigate the effects of IL-27 on ovalbumin (OVA)-challenged asthmatic mice in vivo and TGF-β1-induced EMT in 16HBE cells in vitro. METHODS: Airway inflammation, mucus secretion, and collagen deposition were analysed by conventional pathological techniques. The ratio of Th17 and Th9 cells in the spleen of mice was measured using flow cytometry, ELISA was performed for cytokine analysis to identify EMT-related molecules and signalling pathways, and other molecular and cellular techniques were used to explore the functional mechanism involving IL-27 and EMT. RESULTS: Airway inflammation in asthmatic mice was significantly alleviated by IL-27, with downregulation of RhoA and ROCK, upregulation of E-cadherin, and a decrease of vimentin and α-SMA expression, compared to asthmatic mice. Moreover, the frequency of Th17 and Th9 cells in the spleen of asthmatic mice decreased following treatment with IL-27. In TGF-β1-induced 16HBE cells, the addition of IL-27 was shown to inhibit EMT, based on the expression of E-cadherin, vimentin, and α-SMA. CONCLUSION: Intranasal administration of IL-27 attenuates airway inflammation and EMT in a murine model of allergic asthma possibly by downregulating the RhoA/ROCK signalling pathway.
KW - asthma
KW - airway remodelling
KW - interleukin 27
KW - epithelial-mesenchymal transition
KW - RhoA/ROCK signalling
DO - 10.1684/ecn.2021.0476