Cellular endotoxin desensitization in patients with severe chronic heart failure

Eur J Heart Fail. 2005 Aug;7(5):865-8. doi: 10.1016/j.ejheart.2004.09.014.

Abstract

Background: Increased levels of bacterial lipopolysaccharide (LPS) have been demonstrated in chronic heart failure (CHF). LPS can induce cellular desensitization, with specific down-regulation of LPS-mediated cellular tumor necrosis factor (TNF-alpha) production which does not affect other cytokine parameters. It is not known if LPS desensitization occurs in CHF.

Methods and results: Mononuclear cells from 24 CHF patients (mean age 70+/-2 years, age range 58 to 78 years, NYHA class 3.0+/-0.2) and 11 healthy controls (mean age 53+/-3 years, age range 39 to 75 years) were separated from venous blood and cultured for 24 h with LPS (E. coli, 0-10 ng/mL). Culture supernatants were tested for TNF-alpha and interleukin-1 receptor antagonist (IL-1RA). Patients were subgrouped into mild (n=10), moderate (n=5), and severe (n=9) CHF. Independently of age, mononuclear cells from patients with severe heart failure produced less TNF-alpha than controls (p<0.05) and patients with mild (p<0.001) or moderate CHF (p<0.05). IL-1RA release was higher for CHF patients as a group, compared with controls (p<0.05). There was no significant difference in IL-1RA release between CHF patient subgroups.

Conclusions: Mononuclear cells from patients with severe heart failure produce significantly less TNF-alpha than healthy controls or patients with mild to moderate disease. Production of IL-1RA is not affected. This resembles a picture indicative of LPS desensitization occurring in patients with severe CHF.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Aged
  • Cells, Cultured
  • Dose-Response Relationship, Drug
  • Endotoxins / blood*
  • Enzyme-Linked Immunosorbent Assay
  • Female
  • Heart Failure / blood*
  • Humans
  • Leukocytes, Mononuclear / metabolism
  • Lipopolysaccharides
  • Male
  • Middle Aged
  • Receptors, Tumor Necrosis Factor / blood
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • Endotoxins
  • Lipopolysaccharides
  • Receptors, Tumor Necrosis Factor
  • Tumor Necrosis Factor-alpha