title: Association of lipopolysaccharide-binding protein and coronary artery disease in men.
abstract: OBJECTIVE
  In this study we tested the hypothesis that lipopolysaccharide-binding protein (LBP) might be able to be used as a biomarker for coronary artery disease (CAD).
  
  
  BACKGROUND
  The mechanisms by which the innate immune recognition of pathogens could lead to atherosclerosis remain unclear. Lipopolysaccharide-binding protein is the first protein to encounter lipopolysaccharide and to deliver it to its cellular targets, toll-like receptors; therefore, its presence might be a reliable biomarker that indicates activation of innate immune responses.
  
  
  METHODS
  A total of 247 men undergoing elective coronary angiography were studied, and the extent of coronary atherosclerosis was assessed by 2 established scores: "extent score" and "severity score." Levels of LBP, markers of inflammation, and traditional risk factors for CAD were assessed.
  
  
  RESULTS
  Serum LBP concentration was significantly increased in 172 patients with angiographically confirmed CAD compared with 75 individuals without coronary atherosclerosis (20.6 +/- 8.7 pg/ml vs. 17.1 +/- 6.0 pg/ml, respectively; p = 0.002). Moreover in multivariable logistic regression analyses, adjusted for established cardiovascular risk factors and markers of systemic inflammation, LBP was a significant and independent predictor of prevalent CAD (p < 0.05 in all models).
  
  
  CONCLUSIONS
  Lipopolysaccharide-binding protein might serve as a novel marker for CAD in men. The present results underlie the potential importance of innate immune mechanisms for CAD. Further studies are warranted to bolster the data and to identify pathogenetic links between innate immune system activation and atherosclerosis.
authors.affiliation: Department of Intensive Care Medicine, University Hospital of Bern (Inselspital), Bern, Switzerland. philipp.lepper@insel.ch
authors.forename: Philipp M
authors.initials: PM
authors.lastname: Lepper
authors.forename: Christian
authors.initials: C
authors.lastname: Schumann
authors.forename: Kathy
authors.initials: K
authors.lastname: Triantafilou
authors.forename: F Maximilian
authors.initials: FM
authors.lastname: Rasche
authors.forename: Tibor
authors.initials: T
authors.lastname: Schuster
authors.forename: Hedwig
authors.initials: H
authors.lastname: Frank
authors.forename: E Marion
authors.initials: EM
authors.lastname: Schneider
authors.forename: Martha
authors.initials: M
authors.lastname: Triantafilou
authors.forename: Maximilian
authors.initials: M
authors.lastname: von Eynatten
mesh_terms: D000209:Acute-Phase Proteins; D000328:Adult; D000367:Age Factors; D000368:Aged; D000369:Aged, 80 and over; D015415:Biomarkers / Q000097:blood; D002352:Carrier Proteins / Q000097:blood*; D016022:Case-Control Studies; D017023:Coronary Angiography; D003327:Coronary Disease / Q000097:blood* / Q000000981:diagnostic imaging / Q000503:physiopathology*; D016207:Cytokines / Q000097:blood; D004797:Enzyme-Linked Immunosorbent Assay; D006801:Humans; D007333:Insulin Resistance; D016015:Logistic Models; D008297:Male; D008562:Membrane Glycoproteins / Q000097:blood*; D008875:Middle Aged; D015999:Multivariate Analysis; D011237:Predictive Value of Tests; D011336:Probability; D011379:Prognosis; D012016:Reference Values; D018570:Risk Assessment; D012680:Sensitivity and Specificity; D012720:Severity of Illness Index; D000099231:Lipopolysaccharide-Binding Protein
chemical_list: D000209:Acute-Phase Proteins; D015415:Biomarkers; D002352:Carrier Proteins; D016207:Cytokines; D008562:Membrane Glycoproteins; D000099231:Lipopolysaccharide-Binding Protein