TNF-α levels are not increased in inflamed patients carrying the CCR5 deletion 32

Cytokine. 2011 Jan;53(1):16-8. doi: 10.1016/j.cyto.2010.09.001. Epub 2010 Oct 6.

Abstract

Background and aims: Recently we reported on a genetically predisposed protection from C-reactive protein (CRP) related mortality in dialysis patients carrying the functional CC-chemokine receptor 5 deletion 32 allele (CCR5Δ32) mutation. Since CCR5Δ32 is associated with a less pro-inflammatory immune response in mice, we hypothesized that the observed protection is (in part) due to a less pro-inflammatory cytokine profile.

Methods: Cross-sectional observational study including 263 incident dialysis patients aged 18-70years, without clinical signs of infection and/or acute vasculitis. TNF-α, IL-6, IL-10 and hsCRP levels were determined and studied in relation to the CCR5 genotype.

Results: In the presence of elevated hsCRP, IL-6 concentration was higher irrespective of the CCR5 genotype. However, in patients with the CCR5 deletion, TNF-α did not differ in the presence/absence of elevated hsCRP and was not correlated with hsCRP levels in carriers of the CCR5Δ32 polymorphism.

Conclusions: A possible underlying mechanism of the impact of CCR5Δ32 genotype on inflammation driven mortality in dialysis patients could be a reduced Th1 immune response as represented by decreased TNF-α levels.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adolescent
  • Adult
  • Aged
  • C-Reactive Protein / metabolism
  • Female
  • Gene Deletion*
  • Genotype
  • Humans
  • Inflammation / blood*
  • Inflammation / genetics*
  • Interleukin-10 / blood
  • Interleukin-6 / blood
  • Male
  • Middle Aged
  • Receptors, CCR5 / genetics*
  • Tumor Necrosis Factor-alpha / blood*
  • Young Adult

Substances

  • Interleukin-6
  • Receptors, CCR5
  • Tumor Necrosis Factor-alpha
  • Interleukin-10
  • C-Reactive Protein