Critical regulation of inflammation via class A scavenger receptor

被引:6
作者
Xie, Liang [1 ]
Li, Qingmin [2 ]
Dong, Ran [3 ]
Zhao, Kaishun [4 ]
Feng, Yun [1 ]
Bao, Zhiyao [1 ]
Zhou, Min [1 ]
机构
[1] Shanghai Jiao Tong Univ, Shanghai Inst Resp Dis, Ruijin Hosp, Dept Pulm & Crit Care Med,Sch Med, 197 Ruijin Er Rd, Shanghai 200025, Peoples R China
[2] Henan Prov Peoples Hosp, Dept Cardiol, Zhengzhou, Henan, Peoples R China
[3] Tongji Univ, Tongji Hosp, Dept Resp Med, Sch Med, Shanghai, Peoples R China
[4] Jiading Cent Hosp, Dept Resp Med, Shanghai, Peoples R China
基金
中国国家自然科学基金;
关键词
chronic obstructive pulmonary disease; class A scavenger receptor; inflammation; cigarette smoke extract; lipopolysaccharides; poly(I:C); H1N1; influenza; OBSTRUCTIVE PULMONARY-DISEASE; LUNG-DISEASE; INFECTION; RECOGNITION; MACROPHAGES; SHOCK; PATHOGENESIS; ACTIVATION; DIAGNOSIS; ASTHMA;
D O I
10.2147/COPD.S153326
中图分类号
R56 [呼吸系及胸部疾病];
学科分类号
摘要
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.
引用
收藏
页码:1145 / 1155
页数:11
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