Abstract
The aryl hydrocarbon receptor (AhR), a transcription factor of the bHLH/PAS family, has recently been demonstrated to regulate T cell differentiation. Whether AhR activation participates in allergic airway inflammation remains unknown. In the current study, using a non-eosinophilic asthma model, we demonstrate that 2, 3, 7, 8-tetrachlorodibenzo-P-dioxin (TCDD), a potent AhR ligand, reduced the airway infiltration of neutrophils, airway hyperresponsiveness and Th17 cytokine expression. Furthermore, stimulation with TCDD promoted Treg differentiation and inhibited Th17 differentiation. However, the maturation of dendritic cells may not be inhibited by AhR activation. This study thus indicates a critical role of TCDD-induced AhR activation in the regulation of non-eosinophilic airway inflammation.
Highlights
Asthma, a complex respiratory disease, is characterized by airway inflammation, bronchial hyperresponsiveness and airway structural remodeling [1, 2]
Activated aryl hydrocarbon receptor (AhR) binds to its dimerization partner, which enhances the expression of the target genes, such as cytochrome P450 1a1 (CYP1a1) and CYP1b1 [12]
These findings suggest that TCDD-induced AhR activation prevents the development of allergen-induced non-eosinophilic airway inflammation and airway hyperresponsiveness
Summary
A complex respiratory disease, is characterized by airway inflammation, bronchial hyperresponsiveness and airway structural remodeling [1, 2]. It is driven by Th2 and Th17 cell differentiation and activation, which leads to eosinophilic and neutrophilic airway infiltration, respectively. Recent studies have demonstrated that neutrophilic airway inflammation primarily occurs in more severe asthma [3, 4, 5]. The functional impairment of regulatory T lymphocytes (Tregs) boosted the activation of effector T lymphocytes via the production of proinflammatory dendritic cells [7, 8]. The effective regulation of T cell differentiation has important value in controlling airway inflammation in asthma
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