Vitamin A–regulated ciliated cells promote airway epithelium repair in an asthma mouse model

• Wen Tan ^[1] ; Jilei Lin ^[2] ; Yaping Wang ^[1] ; Li Yan ^[1] ; Linyan Ying ^[1] ; Jihong Dai ^[1] ; Zhou Fu ^[1] ; Jingyue Liu ^[1]
  1. [1] National Clinical Research Center for Child Health and Disorders, Ministry of Education Key Laboratory of Child Development and Disorders, Chongqing Key Laboratory of Pediatrics, Children’s Hospital of Chongqing Medical University, Chongqing, China
  2. [2] National Clinical Research Center for Child Health and Disorders, Ministry of Education Key Laboratory of Child Development and Disorders, Chongqing Key Laboratory of Pediatrics, Children’s Hospital of Chongqing Medical University, Chongqing, China; Department of Respiratory Medicine, Children’s Hospital of Chongqing Medical University, Chongqing, China.
• Localización: Allergologia et immunopathologia: International journal for clinical and investigate allergology and clinical immunology, ISSN-e 1578-1267, ISSN 0301-0546, Vol. 51, Nº. 1, 2023, págs. 116-125
• Idioma: inglés
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• Resumen

  • Background: Asthma is a chronic inflammatory airway disease that causes damage to and exfoliation of the airway epithelium. The continuous damage to the airway epithelium in asthma cannot be repaired quickly and generates irreversible damage, repeated attacks, and aggravation. Vitamin A (VA) has multifarious biological functions that include maintaining membrane stability and integrity of the structure and function of epithelial cells. Our research explored the role of VA in repairing the airway epithelium and provided a novel treatment strategy for asthma.

    Methods: A mouse asthma model was established by house dust mite (HDM) and treated with VA by gavage. Human bronchial epithelial (16HBE) cells were treated with HDM and all-trans retinoic acid (ATRA) in vitro. We analyzed the mRNA and protein expression of characteristic markers, such as acetyl-α-tubulin (Ac-TUB) and FOXJ1 in ciliated cells and MUC5AC in secretory cells, mucus secretion, airway inflammation, the morphology of cilia, and the integrity of the airway epithelium.

    Results: Findings showed destruction of airway epithelial integrity, damaged cilia, high mucus secretion, increased MUC5AC expression, and decreased Ac-TUB and FOXJ1 expression in asthmatic mice. The VA intervention reversed the effect on Ac-TUB and FOXJ1 and promoted ciliated cells to repair the damage and maintain airway epithelial integrity. In 16HBE cells, we could confirm that ATRA promoted the expression of Ac-TUB and FOXJ1.

    Conclusion: These results demonstrated that VA-regulated ciliated cells to repair the damaged airway epithelium caused by asthma and maintain airway epithelial integrity. VA intervention is a potential adjunct to conventional treatment for asthma.