title: Decreased plasma IL-35 levels are related to the left ventricular ejection fraction in coronary artery diseases.
abstract: BACKGROUND
  Accumulating evidence shows that the novel anti-inflammatory cytokine IL-35 can efficiently suppress effector T cell activity and alter the progression of inflammatory and autoimmune diseases. The two subunits of IL-35, EBI3 and p35, are strongly expressed in human advanced plaque, suggesting a potential role of IL-35 in atherosclerosis and coronary artery disease (CAD). However, the plasma levels of IL-35 in patients with CAD have yet to be investigated.
  
  
  METHODS
  Plasma IL-35, IL-10, TGF-β1, IL-12 and IL-27 levels were measured using an ELISA in 43 stable angina pectoris (SAP) patients, 62 unstable angina pectoris (UAP) patients, 56 acute myocardial infarction (AMI) patients and 47 chest pain syndrome patients as a control group.
  
  
  RESULTS
  The results showed that plasma IL-35 levels were significantly decreased in the SAP group (90.74±34.22 pg/ml), the UAP group (72.20±26.63 pg/ml), and the AMI group (50.21±24.69 pg/ml) compared with chest pain syndrome group (115.06±32.27 pg/ml). Similar results were also demonstrated with IL-10 and TGF-β1. Plasma IL-12 and IL-27 levels were significantly increased in the UAP group (349.72±85.22 pg/ml, 101.75±51.42 pg/ml, respectively) and the AMI group (318.05±86.82 pg/ml, 148.88±68.45 pg/ml, respectively) compared with chest pain syndrome group (138.68±34.37 pg/ml, 63.60±22.75 pg/ml, respectively) and the SAP group (153.84±53.86 pg/ml, 70.84±38.77 pg/ml, respectively). Furthermore, lower IL-35 levels were moderately positively correlated with left ventricular ejection fraction (LVEF) in CAD patients (R = 0.416, P<0.01), whereas higher IL-27 levels were weakly negatively correlated with LVEF in CAD patients(R = -0.205, P<0.01).
  
  
  CONCLUSIONS
  The results of the present study show that circulating IL-35 is a potentially novel biomarker for coronary artery disease. Regulating the expression of IL-35 also provides a new possible target for the treatment of atherosclerosis and CAD.
authors.affiliation: Department of Cardiology, the People's Hospital of Guangxi Zhuang Autonomous Region, Nanning, China.
authors.forename: Yingzhong
authors.initials: Y
authors.lastname: Lin
authors.forename: Ying
authors.initials: Y
authors.lastname: Huang
authors.forename: Zhengde
authors.initials: Z
authors.lastname: Lu
authors.forename: Cheng
authors.initials: C
authors.lastname: Luo
authors.forename: Ying
authors.initials: Y
authors.lastname: shi
authors.forename: Qiutang
authors.initials: Q
authors.lastname: Zeng
authors.forename: Yifeng
authors.initials: Y
authors.lastname: Cao
authors.forename: Lin
authors.initials: L
authors.lastname: Liu
authors.forename: Xiaoyan
authors.initials: X
authors.lastname: Wang
authors.forename: Qingwei
authors.initials: Q
authors.lastname: Ji
mesh_terms: D001241:Aspirin / Q000494:pharmacology; D000077144:Clopidogrel; D003324:Coronary Artery Disease / Q000097:blood* / Q000503:physiopathology*; D016207:Cytokines / Q000097:blood; D005260:Female; D006801:Humans; D007378:Interleukins / Q000097:blood*; D008297:Male; D008875:Middle Aged; D018709:Statistics, Nonparametric; D013318:Stroke Volume / Q000187:drug effects; D013988:Ticlopidine / Q000031:analogs & derivatives / Q000494:pharmacology
chemical_list: D016207:Cytokines; D007378:Interleukins; C464565:MYDGF protein, human; C532417:interleukin-35, human; D000077144:Clopidogrel; D013988:Ticlopidine; D001241:Aspirin