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- Title
KIF2A decreases IL-33 production and attenuates allergic asthmatic inflammation.
- Authors
Wang, Zhengxia; Wu, Jingjing; Jiang, Jingxian; Ma, Qiyun; Song, Meijuan; Xu, Tingting; Liu, Yanan; Chen, Zhongqi; Bao, Yanmin; Huang, Mao; Zhang, Mingshun; Ji, Ningfei
- Abstract
Background: The microtubule-dependent molecular motor protein Kinesin Family Member 2A (KIF2A) is down-regulated in asthmatic human airway epithelium. However, little is known about the roles of KIF2A as well as the possible underlying mechanisms in asthma. Methods: House dust mite (HDM) extract was administered to establish a murine model of asthma. The expression of KIF2A, IL-33 and the autophagy pathways were detected. The plasmid pCMV-KIF2A was used to overexpress KIF2A in the airway epithelial cells in vitro and in vivo. IL-4, IL-5, IL-33 and other cytokines in bronchoalveolar lavage fluid (BALF) and lung tissues homogenates were measured. Results: In response to the challenge of house dust mite (HDM) in vitro and in vivo, airway epithelial cells displayed decreased production of KIF2A. Meanwhile, autophagy and IL-33 were increased in HMD-treated epithelial cells. Mechanistically, KIF2A decreased autophagy via suppressing mTORC1 pathway in HDM-treated epithelial cells, which contributed to the reduced production of IL-33. Moreover, in vivo KIF2A transfection reduced IL-33 and autophagy in the lung, leading to the attenuation of allergic asthma. Conclusion: KIF2A suppressed mTORC1-mediated autophagy and decreased the production of epithelial-derived cytokine IL-33 in allergic airway inflammation. These data indicate that KIF2A may be a novel target in allergic asthma.
- Subjects
MOLECULAR motor proteins; INTERLEUKIN-33; HOUSE dust mites; EPITHELIAL cells; AIRWAY (Anatomy)
- Publication
Allergy, Asthma & Clinical Immunology, 2022, Vol 18, Issue 1, p1
- ISSN
1710-1484
- Publication type
Article
- DOI
10.1186/s13223-022-00697-9