International Journal of COPD (Apr 2018)

Critical regulation of inflammation via class A scavenger receptor

  • Xie L,
  • Li Q,
  • Dong R,
  • Zhao K,
  • Feng Y,
  • Bao Z,
  • Zhou M

Journal volume & issue
Vol. Volume 13
pp. 1145 – 1155

Abstract

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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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