title: Upregulation of monocyte proinflammatory cytokine production by C-reactive protein is significantly related to ongoing myocardial damage and future cardiac events in patients with chronic heart failure.
abstract: BACKGROUND
  An elevation of the cardiac troponin T (TnT) level identifies patients with ongoing myocardial damage (OMD) and at increased risk for future cardiac events in chronic heart failure (CHF). C-reactive protein (CRP) upregulates monocyte proinflammatory cytokine production and this upregulation appears to play an important role on OMD.
  
  
  RESULTS
  Peripheral blood mononuclear cells (PBMCs) were stimulated by 25 microg/mL CRP in 72 patients with CHF. Tumor necrosis factor (TNF)-alpha and interleukin (IL)-6 production by monocytes was measured by a specific enzyme-linked immunosorbent assay and expressed as the mean +/- SD (pg x mL x 10(6) PBMCs). The patients were divided into 2 groups according to the TnT levels: 27 patients with OMD (TnT >/= 0.01 ng/mL) and 45 patients without OMD. CRP-induced cytokine production was upregulated significantly more in patients with OMD than in those without OMD (TNF-alpha: 200.6 +/- 100.4 vs. 102.1 +/- 73.6 pg/mL, P < .001, IL-6: 4611.7 +/- 2600.0 vs. 1451.6 +/- 1193.5 pg/mL, P < .001). Multivariate Cox regression analyses revealed that CRP-stimulated monocyte production of TNF-alpha >/= 120 pg/mL and TnT >/= 0.03 ng/mL were independent predictors of cardiac events.
  
  
  CONCLUSIONS
  The upregulation of monocyte proinflammatory cytokine production by CRP could be significantly related to OMD and future cardiac events in CHF.
authors.affiliation: Department of Cardiology, Tama-Nagayama Hospital, Nippon Medical School, Tokyo, Japan. Nakagomi@nms.ac.jp
authors.forename: Akihiro
authors.initials: A
authors.lastname: Nakagomi
authors.forename: Yoshihiko
authors.initials: Y
authors.lastname: Seino
authors.forename: Yasumi
authors.initials: Y
authors.lastname: Endoh
authors.forename: Yoshiki
authors.initials: Y
authors.lastname: Kusama
authors.forename: Hirotsugu
authors.initials: H
authors.lastname: Atarashi
authors.forename: Kyoichi
authors.initials: K
authors.lastname: Mizuno
mesh_terms: D000368:Aged; D002097:C-Reactive Protein / Q000502:physiology*; D016207:Cytokines / Q000096:biosynthesis / Q000097:blood*; D005260:Female; D005500:Follow-Up Studies; D006333:Heart Failure / Q000097:blood* / Q000473:pathology; D006801:Humans; D007963:Leukocytes, Mononuclear / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D009000:Monocytes / Q000378:metabolism*; D009206:Myocardium / Q000378:metabolism* / Q000473:pathology; D015854:Up-Regulation / Q000502:physiology*
chemical_list: D016207:Cytokines; D002097:C-Reactive Protein