Critical regulation of inflammation via class A scavenger receptor.
Critical regulation of inflammation via class A scavenger receptor.
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通过 A 类清道夫受体对炎症进行关键调节
DOI：
10.2147/copd.s153326
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发表时间：
2018
影响因子：
2.8
通讯作者：
Zhou M
中科院分区：
文献类型：
--
作者：
Xie L;Li Q;Dong R;Zhao K;Feng Y;Bao Z;Zhou M
炎症是慢性阻塞性肺病的重要病因。肺泡巨噬细胞是在COPD病理中起重要作用的主要先天免疫细胞。A类清道夫受体（Class A scavenger receptor, SR-A）是巨噬细胞表达的一种模式识别受体。本研究探讨了SR-A通过调节炎症在COPD进展中的作用。采用免疫组织化学、免疫荧光和实时荧光定量PCR检测COPD患者和对照组（吸烟者和未患COPD的非吸烟者）SR-A的表达。采用酶联免疫吸附法检测BAL细胞因子水平。为了进一步证明我们的假设，我们用脂多糖、聚（I:C）、香烟烟雾提取物和从患者分离的H1N1流感病毒处理过表达SR-A的RAW264.7细胞24小时，并检测炎症细胞因子的水平。结果COPD和非COPD吸烟者肺泡巨噬细胞中SR-A表达水平均上调。SR-A mRNA水平与COPD患者炎症因子呈正相关，与预测FEV1%呈负相关。在RAW-SR-A细胞中，炎症因子水平明显高于对照组。结论SR-A可增加香烟烟雾提取物、细菌和病毒刺激的炎症，导致COPD患者长期炎症，可能成为COPD治疗的新靶点。
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.
A 类清道夫受体在自身免疫 NOD 小鼠糖尿病发展中的双重作用。
影响因子：
3.7
作者：
Shimizu M;Yasuda H;Hara K;Takahashi K;Nagata M;Yokono K
通讯作者：
Yokono K