impact factor, citescore
logo
 

Full Papers

 

Aromatic hydrocarbon receptor provides a link between smoking and rheumatoid arthritis in peripheral blood mononuclear cells


1, 2, 3, 4, 5

 

  1. Department of Rheumatology and Immunology, The Second Hospital of Anhui Medical University, Anhui, China.
  2. Department of Rheumatology and Immunology, The Second Hospital of Anhui Medical University, Anhui, China. longqian0551@hotmail.com
  3. Department of Rheumatology and Immunology, The Second Hospital of Anhui Medical University, Anhui, China.
  4. Department of Rheumatology and Immunology, The Second Hospital of Anhui Medical University, Anhui, China.
  5. Department of Rheumatology and Immunology, The Second Hospital of Anhui Medical University, Anhui, China.

CER11244
2019 Vol.37, N°3
PI 0445, PF 0449
Full Papers

Free to view
(click on article PDF icon to read the article)

PMID: 30418118 [PubMed]

Received: 13/03/2018
Accepted : 18/07/2018
In Press: 22/10/2018
Published: 10/05/2019

Abstract

OBJECTIVES:
Epidemiology shows that smoking plays a central role in rheumatoid arthritis (RA). The aim of this study was to evaluate the potential relationship between smoking, aromatic hydrocarbon receptor (AHR) and RA susceptibility.
METHODS:
We performed a hospital-based, case-control study of patients with RA and healthy controls. Expressions of AHR, cytochrome P4501A1(CYP1A1), aromatic hydrocarbon receptor repressor (AHRR) genes were assessed in peripheral blood mononuclear cells (PBMCs) and cultured cells using real-time PCR. The response of PBMCs to the AHR agonist, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and cigarette smoke extract (CSE) were cultured in vitro.
RESULTS:
AHR and its downstream gene expressions were demonstrated in smoking rheumatoid PBMCs and non-smoking patients with significantly higher expression in smoking patients. The observation was consistent with the sensitivity of RA PBMCs to TCDD and CSE stimulation demonstrated in vitro.
CONCLUSIONS:
Our study shows that smoking may be involved in the pathogenesis of RA by the AHR pathway.

Rheumatology Article