PMID- 15982613
OWN - NLM
STAT- MEDLINE
DCOM- 20060713
LR  - 20171116
IS  - 1053-2498 (Print)
IS  - 1053-2498 (Linking)
VI  - 24
IP  - 7
DP  - 2005 Jul
TI  - Intracellular monocyte cytokine production and CD 14 expression are up-regulated 
      in severe vs mild chronic heart failure.
PG  - 854-9
AB  - BACKGROUND: The role of circulating monocytes in the process of low-grade 
      inflammation, characteristic of chronic heart failure (CHF), has recently been 
      questioned. Lipopolysaccharide (LPS) desensitization has been proposed to mediate 
      reduced monocyte cytokine elaboration in patients with severe CHF. METHODS: 
      Intracellular monocyte production of interleukin-1 beta (IL-1 beta), 
      interleukin-6 (IL-6) and tumor necrosis factor (TNF)-alpha, and monocyte CD 14 
      expression were measured flow-cytometrically without and after 8-hour LPS 
      stimulation in 46 patients with CHF and in a healthy control group. RESULTS: 
      Basal cytokine concentrations were similar for the control and the mild CHF 
      groups (New York Heart Association [NYHA] Class I or II). After LPS stimulation, 
      IL-6 (p=0.002) and TNF-alpha levels (p=0.001) were lower in the latter group, 
      whereas IL-1 beta production was comparable. For the moderate-severe CHF 
      patients, unstimulated IL-1 beta (p=0.04) was higher, whereas IL-6 (p=0.2) and 
      TNF-alpha (p=0.1) levels were not different from the controls. Measurement of 
      LPS-stimulated cytokine production showed no differences between the control 
      group and patients with moderate-severe CHF (all p= 0.5). Upon comparing mild vs 
      moderate-severe CHF patients, higher levels of unstimulated cytokine production 
      (IL-1 beta, p=0.002; IL-6, p=0.01; TNF-alpha, p=0.003), stimulated IL-1 beta 
      (p=0.002) and IL-6 (p=0.008) were found in the latter patients. CD 14 expression 
      in the moderate-severe CHF group was higher than in the mild-CHF group (p = 0.03) 
      and was strongly related to stimulated IL-1 beta (r=0.62, p<0.0001), IL-6 
      (r=0.56, p=0.0002) and TNF-alpha (r=0.41, p=0.006) production. CONCLUSIONS: CD 14 
      expression and monocyte cytokine production, both unstimulated and after LPS 
      stimulation, are increased in moderate-severe CHF when compared with mild CHF. 
      These data suggest that circulating monocytes, possibly via increased CD 14 
      expression, may play a significant role in the immunologic dysbalance observed in 
      advanced CHF.
FAU - Conraads, Viviane M
AU  - Conraads VM
AD  - Department of Cardiology, University Hospital Antwerp (UIA), Antwerp, Belgium. 
      viviane.conrads@uza.be
FAU - Bosmans, Johan M
AU  - Bosmans JM
FAU - Schuerwegh, Annemie J
AU  - Schuerwegh AJ
FAU - Goovaerts, Inge
AU  - Goovaerts I
FAU - De Clerck, Luc S
AU  - De Clerck LS
FAU - Stevens, Wim J
AU  - Stevens WJ
FAU - Bridts, Chris H
AU  - Bridts CH
FAU - Vrints, Christiaan J
AU  - Vrints CJ
LA  - eng
PT  - Journal Article
PL  - United States
TA  - J Heart Lung Transplant
JT  - The Journal of heart and lung transplantation : the official publication of the 
      International Society for Heart Transplantation
JID - 9102703
RN  - 0 (Cytokines)
RN  - 0 (Interleukin-6)
RN  - 0 (Lipopolysaccharide Receptors)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (Receptors, Tumor Necrosis Factor, Type I)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 0 (Tumor Necrosis Factors)
SB  - IM
MH  - Cytokines/biosynthesis/*metabolism
MH  - Female
MH  - Heart Failure/blood/*metabolism
MH  - Humans
MH  - Interleukin-6/biosynthesis
MH  - Lipopolysaccharide Receptors/*biosynthesis
MH  - Lipopolysaccharides
MH  - Male
MH  - Middle Aged
MH  - Monocytes/*metabolism
MH  - Receptors, Tumor Necrosis Factor, Type I/metabolism
MH  - Tumor Necrosis Factor-alpha/metabolism
MH  - Tumor Necrosis Factors/metabolism
EDAT- 2005/06/29 09:00
MHDA- 2006/07/14 09:00
CRDT- 2005/06/29 09:00
PHST- 2003/10/08 00:00 [received]
PHST- 2004/03/23 00:00 [revised]
PHST- 2004/04/12 00:00 [accepted]
PHST- 2005/06/29 09:00 [pubmed]
PHST- 2006/07/14 09:00 [medline]
PHST- 2005/06/29 09:00 [entrez]
AID - S1053-2498(04)00271-2 [pii]
AID - 10.1016/j.healun.2004.04.017 [doi]
PST - ppublish
SO  - J Heart Lung Transplant. 2005 Jul;24(7):854-9. doi: 10.1016/j.healun.2004.04.017.