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Tytuł pozycji:

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

Tytuł:
[Aryl hydrocarbon receptor modulates airway inflammation in mice with cockroach allergen-induced asthma by regulating Th17/Treg differentiation].
Autorzy:
Xu T; Sleep Medicine Center, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.
Cui Z; Department of Orthopedics and Traumatology, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.
Wang J; Second Affiliated Hospital of Guangzhou Medical University, Guangzhou 510260, China.
Feng Y; Sleep Medicine Center, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.
Xie R; Sleep Medicine Center, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.
Li D; Sleep Medicine Center, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.
Peng J; Sleep Medicine Center, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.
Huang R; Sleep Medicine Center, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.
Li T; Sleep Medicine Center, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.
Źródło:
Nan fang yi ke da xue xue bao = Journal of Southern Medical University [Nan Fang Yi Ke Da Xue Xue Bao] 2021 May 20; Vol. 41 (5), pp. 716-721.
Typ publikacji:
Journal Article
Język:
Chinese
Imprint Name(s):
Original Publication: Guangzhou : Nanfang yi ke da xue xue bao bian ji bu, 2005-
MeSH Terms:
Asthma*/chemically induced
Asthma*/drug therapy
Cockroaches*
Allergens ; Animals ; Cell Differentiation ; Inflammation ; Mice ; Receptors, Aryl Hydrocarbon/genetics ; T-Lymphocytes, Regulatory ; Th17 Cells
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Contributed Indexing:
Keywords: Aryl hydrocarbon receptor; Th17; Treg; asthma; cockroach allergen
Substance Nomenclature:
0 (Allergens)
0 (Receptors, Aryl Hydrocarbon)
Entry Date(s):
Date Created: 20210617 Date Completed: 20210618 Latest Revision: 20210718
Update Code:
20240104
PubMed Central ID:
PMC8214952
DOI:
10.12122/j.issn.1673-4254.2021.05.12
PMID:
34134959
Czasopismo naukowe
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 < 0.002). TCDD treatment significantly decreased inflammatory cells and mucus production in the lungs of asthmatic mice, and BALFs from TCDD-treated mice with CRE challenge contained lowered levels of the proinflammatory factors including IL-4, IL-13 and IL-17A ( P < 0.001) but increased anti-inflammatory factors including IL-10, IL-22 and TGF-β1 ( P < 0.001). All these changes were significantly reversed by treatment with CH223191 to the levels comparable with those in the asthma model group ( 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 < 0.001); inhibition of AhR with CH223191, as compared with TCDD, significantly decreased the expression of CD4 + CD25 + Foxp3 + Treg cells in the lungs and pulmonary lymph nodes and the expression of FOXP3 mRNA in lymphocytes and increased RORγt mRNA expression ( P < 0.001) to the levels comparable with those in asthma model group ( P >0.05).
Objective: AhR activation modulates airway inflammation in mice with CRE-induced asthma by modulating the differentiation of Th17/Treg.

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