Critical regulation of inflammation via class A scavenger receptor
Authors Xie L, Li Q, Dong R, Zhao K, Feng Y, Bao Z, Zhou M
Received 5 October 2017
Accepted for publication 24 February 2018
Published 13 April 2018 Volume 2018:13 Pages 1145—1155
Checked for plagiarism Yes
Review by Single-blind
Peer reviewers approved by Dr Charles Downs
Peer reviewer comments 3
Editor who approved publication: Prof. Dr. Chunxue Bai
Liang Xie,1,* Qingmin Li,2,* Ran Dong,3,* Kaishun Zhao,4 Yun Feng,1 Zhiyao Bao,1 Min Zhou1
1Department of Pulmonary and Critical Care Medicine, Shanghai Institute of Respiratory Disease, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China; 2Department of Cardiology, Henan Provincial Peoples Hospital, Zhengzhou, China; 3Department of Respiratory Medicine, Tongji Hospital, Tongji University School of Medicine, Shanghai, China; 4Department of Respiratory Medicine, Jiading Central Hospital, Shanghai, China
*These authors contributed equally to this work
Background: Inflammation is an important cause of COPD. Alveolar macrophages are the major innate immune cells that have an important role in COPD pathology. Class A scavenger receptor (SR-A) is a pattern recognition receptor expressed on macrophages. This study investigates the role of SR-A in COPD progression via regulation of inflammation.
Patients and methods: SR-A expression in COPD patients and control subjects (smokers and nonsmokers without COPD) was measured by immunohistochemistry, immunofluorescence, and real-time PCR. The cytokine levels in BAL were measured by enzyme-linked immunosorbent assay. To further prove our hypothesis, we treated RAW264.7 cells that overexpress SR-A with lipopolysaccharides, poly(I:C), cigarette smoke extract, and H1N1 influenza separated from patients for 24 h and examined the levels of inflammatory cytokines.
Results: In both groups, COPD and smokers without COPD, SR-A expression level was upregulated in alveolar macrophages. SR-A mRNA level was positively correlated with inflammatory cytokines and negatively correlated with FEV1% predicted in COPD patients. In RAW-SR-A cells, level of inflammatory cytokines was significantly higher when compared with control ones.
Conclusion: SR-A could increase inflammation stimulated by cigarette smoke extracts, bacteria, and virus, leading to long-term inflammation in COPD, and thus might be used as a new therapeutic target for COPD treatment.
Keywords: chronic obstructive pulmonary disease, class A scavenger receptor, inflammation, cigarette smoke extract, lipopolysaccharides, poly(I:C), H1N1 influenza
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