[Aryl hydrocarbon receptor modulates airway inflammation in mice with cockroach allergen-induced asthma by regulating Th17/Treg differentiation].

Objective To investigate whether aryl hydrocarbon receptor (AhR) modulates cockroach allergen (CRE)-induced asthma by regulating Th17/Treg differentiation. Objective Mouse models of CRE-induced asthma established by sensitizing and challenging the mice with CRE were randomized into asthma model group, AhR agonist group treated with TCDD (10 μg/ kg), and AhR antagonist group treated with TCDD and CH223191 (10 mg/kg) (n=5), with 5 mice without CRE challenge as the control group. The expressions of AhR, Cyp1a1 and Cyp1b1 mRNA in the lung tissues of the mice were detected using RT-PCR, and pulmonary inflammation was evaluated with immumohistochemical staining. The expressions of inflammatory cytokines in the lungs were detected using ELISA, and the expression of Treg in the lung tissues and pulmonary lymph nodes was analyzed with flow cytometry. Objective Both TCDD and CH223191 were capable of modulating pulmonary expressions of AhR and its downstream genes Cyp1a1 and Cyp1b1 in asthmatic mice (P 0.05). More importantly, TCDD treatment significantly increased the number of Tregs cells and FOXP3 expression and lowered RORγt mRNA expression in the lungs and pulmonary lymph nodes in asthmatic mice (P 0.05). Objective AhR activation modulates airway inflammation in mice with CRE-induced asthma by modulating the differentiation of Th17/Treg.