• 1. Department of Human Anatomy, Jinzhou Medical University, Jinzhou, Liaoning 121000, P. R. China;
  • 2. Department of Thoracic Surgery , Fushun City Central Hospital, Fushun, Liaoning 113006, P. R. China;
  • 3. Department of Developmental Biology, Jinzhou Medical University, Jinzhou, Liaoning 121000, P. R. China;
YAN Wenzhu, Email: 934390583@qq.com
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ObjectiveTo observe repairing process of trachea epithelium cells in chlorine-induced airway epithelial injury.MethodsTwelve mice were exposed to chlorine gas and prepared the mice model of airway damage. Three mice were executed respectively on 2nd, 4th, 7th, 10th day after exposure to chlorine gas, and tracheal tissues were collected. In addition 3 normal mice served as control. Airway repair and cell proliferation were detected by EdU labeling method. The basal cell markers keratin 5 (K5), keratin 14 (K14) were adopted as the tracheal epithelial markers for locating the position of the proliferation of repairing cells. Morphological analysis was adopted to measure the proliferation rate as well as the recovery of the false stratified epithelium.ResultsIn the control group, cell proliferation rate was very low, all basal cells expressed K5, and most basal cells did not express K14. Most of epithelial cells shed from the trachea epithelium after exposure to chlorine gas. 2-4 days after chlorine exposure, K5 and K14 expression basal cells increased, K14 expression cells increased greatly. In the peak period of cell proliferation, only a small number of ciliated cells appeared in the repairing trachea area. Epithelial cells repaired fast and widely at the bottom of the trachea.ConclusionThe trachea residual basal cells play roles of progenitor cells and repair the airway epithelium after chlorine damage in mice.

Citation: WANG Cheng, MA Yunsheng, YAN Wenzhu. Repairing mechanism of chlorine-induced airway epithelial injury: a morphological study. Chinese Journal of Respiratory and Critical Care Medicine, 2018, 17(1): 76-80. doi: 10.7507/1671-6205.201706041 Copy

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