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Critical regulation of inflammation via class A scavenger receptor

Liang Xie1, Qingmin Li2, Ran Dong3

  • 1Department of Pulmonary and Critical Care Medicine, Shanghai Institute of Respiratory Disease, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China.

International Journal of Chronic Obstructive Pulmonary Disease
|April 27, 2018
PubMed
Abstract

Insights

Class A scavenger receptor (SR-A) is upregulated in COPD, increasing inflammation from various triggers. Targeting SR-A may offer a new therapeutic strategy for chronic obstructive pulmonary disease (COPD) treatment.

Area of Science:

  • Immunology
  • Pulmonology
  • Cell Biology

Background:

  • Chronic obstructive pulmonary disease (COPD) is significantly driven by inflammation.
  • Alveolar macrophages are key innate immune cells implicated in COPD pathogenesis.
  • Class A scavenger receptor (SR-A) is a macrophage-expressed pattern recognition receptor.

Purpose of the Study:

  • To investigate the role of SR-A in COPD progression.
  • To determine if SR-A regulates inflammation in COPD.

Main Methods:

  • Measured SR-A expression in COPD patients and controls using immunohistochemistry, immunofluorescence, and real-time PCR.
  • Quantified cytokine levels in bronchoalveolar lavage (BAL) fluid via ELISA.
  • Stimulated RAW264.7 cells overexpressing SR-A with various inflammatory agents (LPS, poly(I:C), CSE, H1N1) and assessed cytokine production.

Main Results:

  • SR-A expression was upregulated in alveolar macrophages of both COPD and smoker control groups.
  • SR-A mRNA levels correlated positively with inflammatory cytokines and negatively with FEV1% predicted in COPD patients.
  • Stimulated RAW-SR-A cells exhibited significantly higher inflammatory cytokine levels compared to controls.

Conclusions:

  • SR-A exacerbates inflammation triggered by cigarette smoke, bacteria, and viruses.
  • SR-A contributes to chronic inflammation in COPD.
  • SR-A presents a potential novel therapeutic target for COPD management.
Keywords:
H1N1 influenzachronic obstructive pulmonary diseasecigarette smoke extractclass A scavenger receptorinflammationlipopolysaccharidespoly(I:C)

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