title: Critical role of RIG-I-like receptors in inflammation in chronic obstructive pulmonary disease.
abstract: BACKGROUND
  Viral infection is a significant cause of chronic obstructive pulmonary disease (COPD) and acute exacerbation of COPD. Retinoic acid inducible gene I (RIG-I)-like receptors (RLRs), including RIG-I and melanoma differentiation associated gene 5 (MDA-5), are important pattern recognition receptors for viral elimination.
  
  
  OBJECTIVE
  The study aims to investigate the role of RIG-I and MDA-5 in COPD pathogenesis.
  
  
  METHODS
  We examined the expression of RIG-I and MDA-5 by immunohistochemistry, real-time PCR and Western blots in COPD patients and control subjects.
  
  
  RESULTS
  Our results showed that MDA-5 expression was upregulated in lung tissues and peripheral blood mononuclear cells of COPD patients and there was a negative correlation between MDA-5 mRNA levels and forced expiratory volume in 1 s %pred. COPD patients had higher interleukin (IL)-1 and IL-8 mRNA expression levels, and these inflammatory cytokines positively correlate with MDA-5 levels. However, there was no difference in the expression of RIG-I between COPD patients and control subjects.
  
  
  CONCLUSIONS
  Our results suggested that MDA-5, but not RIG-I, may play a critical role in airway inflammation in COPD.
authors.affiliation: Department of Respiratory Medicine, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China.
authors.forename: Qiurui
authors.initials: Q
authors.lastname: Zhang
authors.affiliation: Department of Respiratory Medicine, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China.
authors.forename: Huanying
authors.initials: H
authors.lastname: Wan
authors.affiliation: Department of Respiratory Medicine, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China.
authors.forename: Shaoguang
authors.initials: S
authors.lastname: Huang
authors.affiliation: Department of Microbiology and Parasitology, Institutes of Medical Sciences, Shanghai Jiaotong University School of Medicine, Shanghai, China.
authors.forename: Yan
authors.initials: Y
authors.lastname: Zhang
authors.affiliation: Department of Microbiology and Parasitology, Institutes of Medical Sciences, Shanghai Jiaotong University School of Medicine, Shanghai, China.
authors.forename: Yanchun
authors.initials: Y
authors.lastname: Wang
authors.affiliation: Department of Microbiology and Parasitology, Institutes of Medical Sciences, Shanghai Jiaotong University School of Medicine, Shanghai, China.
authors.forename: Xiaokui
authors.initials: X
authors.lastname: Guo
authors.affiliation: Department of Microbiology and Parasitology, Institutes of Medical Sciences, Shanghai Jiaotong University School of Medicine, Shanghai, China.
authors.forename: Ping
authors.initials: P
authors.lastname: He
authors.affiliation: Department of Respiratory Medicine, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China.
authors.forename: Min
authors.initials: M
authors.lastname: Zhou
mesh_terms: D000368:Aged; D000071457:DEAD Box Protein 58; D053487:DEAD-box RNA Helicases / Q000096:biosynthesis* / Q000235:genetics / Q000378:metabolism; D005260:Female; D005541:Forced Expiratory Volume / Q000502:physiology; D006801:Humans; D007249:Inflammation / Q000235:genetics / Q000378:metabolism*; D000072640:Interferon-Induced Helicase, IFIH1; D007375:Interleukin-1 / Q000096:biosynthesis / Q000235:genetics; D016209:Interleukin-8 / Q000096:biosynthesis / Q000235:genetics; D008297:Male; D008875:Middle Aged; D029424:Pulmonary Disease, Chronic Obstructive / Q000235:genetics / Q000378:metabolism* / Q000503:physiopathology; D011971:Receptors, Immunologic; D015854:Up-Regulation
chemical_list: D007375:Interleukin-1; D016209:Interleukin-8; D011971:Receptors, Immunologic; C452820:RIGI protein, human; C452815:IFIH1 protein, human; D000071457:DEAD Box Protein 58; D053487:DEAD-box RNA Helicases; D000072640:Interferon-Induced Helicase, IFIH1
keywords: MDA-5; RIG-I; RIG-I-like receptors; airway inflammation; nic obstructive pulmonary disease