FGF2 is overexpressed in asthma and promotes airway inflammation through the FGFR/MAPK/NF-κB pathway in airway epithelial cells

• Published in: Military medical research 2022-01, Vol.9 (1), p.7-7, Article 7
• Main Authors: Tan, Yuan-Yang, Zhou, Hui-Qin, Lin, Yu-Jing, Yi, Liu-Tong, Chen, Zhuang-Gui, Cao, Qing-Dong, Guo, Yan-Rong, Wang, Zhao-Ni, Chen, Shou-Deng, Li, Yang, Wang, De-Yun, Qiao, Yong-Kang, Yan, Yan
• Format: Article
• Language: English
• Subjects: Airway epithelial cell; Airway inflammation; Animals; Asthma; Asthma - metabolism; Asthma - pathology; Epithelial Cells - metabolism; Fibroblast growth factor 2 (FGF2); Fibroblast Growth Factor 2 - metabolism; Fibroblast Growth Factor 2 - pharmacology; Fibroblasts; Growth factors; House dust mite chronic model; Humans; Inflammation; Inflammation - metabolism; Inflammatory diseases; Laboratory animals; Mice; Mitogen-Activated Protein Kinases - metabolism; NF-kappa B - metabolism; Receptors, Fibroblast Growth Factor - metabolism; Signal transduction; Steroids
• ISSN: 2054-9369; 2095-7467; 2054-9369
• DOI: 10.1186/s40779-022-00366-3

Airway inflammation is the core pathological process of asthma, with the key inflammatory regulators incompletely defined. Recently, fibroblast growth factor 2 (FGF2) has been reported to be an inflammatory regulator; however, its role in asthma remains elusive. This study aimed to investigate the immunomodulatory role of FGF2 in asthma. First, FGF2 expression was characterised in clinical asthma samples and the house dust mite (HDM)-induced mouse chronic asthma model. Second, recombinant mouse FGF2 (rm-FGF2) protein was intranasally delivered to determine the effect of FGF2 on airway inflammatory cell infiltration. Third, human airway epithelium-derived A549 cells were stimulated with either HDM or recombinant human interleukin-1β (IL-1β) protein combined with or without recombinant human FGF2. IL-1β-induced IL-6 or IL-8 release levels were determined using enzyme-linked immunosorbent assay, and the involved signalling transduction was explored via Western blotting. Compared with the control groups, the FGF2 protein levels were significantly upregulated in the bronchial epithelium and alveolar areas of clinical asthma samples (6.70 ± 1.79 vs. 16.32 ± 2.40, P = 0.0184; 11.20 ± 2.11 vs. 21.00 ± 3.00, P = 0.033, respectively) and HDM-induced asthmatic mouse lung lysates (1.00 ± 0.15 vs. 5.14 ± 0.42, P