Role of transient receptor potential cation channel subfamily V member 1 (TRPV1) on ozone-exacerbated allergic asthma in mice. (April 2019)

• Record Type: Journal Article
• Authors: Li, Jinquan; Chen, Yushan; Chen, Qiao Yi; Liu, Dan; Xu, Lang; Cheng, Guirong; Yang, Xu; Guo, Zhenzhong; Zeng, Yan
• Is Part Of: Environmental pollution. Volume 247(2019)
• Page Start: 586
• Page End: 594
• Publication Date: 2019-04
• Subjects: Ozone -- Allergic asthma -- Transient receptor potential cation channel subfamily V member1 -- Calcitonin gene-related peptide -- Thymic stromal lymphopoietin; Pollution -- Periodicals; Pollution -- Environmental aspects -- Periodicals; Environmental Pollution -- Periodicals; Pollution -- Périodiques; Pollution -- Aspect de l'environnement -- Périodiques; Pollution -- Effets physiologiques -- Périodiques; Pollution; Pollution -- Environmental aspects; Periodicals; Electronic journals; 363.73
• DOI: 10.1016/j.envpol.2019.01.091
• Languages: English
• ISSNs: 0269-7491

Abstract

Abstract: Around the globe, worsening air pollution is spawning major public health and environmental concerns, especially in the poorest and most populous cities. As a major secondary air pollutant, ozone is a potential risk factor for exacerbated asthma, although the underlying mechanisms remain uncertain. In this study, we aim to investigate the role of ozone on asthma exacerbation using a classic asthmatic model with allergic airway inflammation by treating Balb/c mice with ovalbumin (OVA). Our study shows ozone exposure significantly exacerbated OVA-induced asthmatic phenotypes, including serum immunoglobulin, Th cytokines, inflammatory cell counts, mucus production, airway remodeling, and airway hyper-responsiveness (AHR). Interestingly, expression of transient receptor potential cation channel subfamily V member1 (TRPV1) was also significantly elevated in ozone-exacerbated asthmatic mice and that treatment with TRPV1 antagonist effectively suppressed AHR, airway inflammation and remodeling. The underlying mechanisms of these effects may be associated with suppression of neuropeptide calcitonin gene-related peptide (CGRP) and thymic stromal lymphopoietin (TSLP), an epithelial cell-derived cytokine. Base on the role of TRPV1 in allergic asthma, this study further revealed that inhibition of TRPV1 by TRPV1 antagonist has significant anti-inflammatory effects on ozone-induced asthma exacerbation in this study. Induction of TRPV1 expression may be an important mechanism underlying the increased risks for asthma after exposure to environmental pollutants. Graphical abstract: Image 1 Highlights: TRPV1 was significantly elevated in ozone-exacerbated asthmatic mice. TRPV1 antagonist effectively suppressed ozone induced exacerbated effect. The underlying mechanisms may be associated with CGRP and TSLP.