The -260 C-->T promoter polymorphism of the lipopolysaccharide receptor CD14 and severe sepsis in trauma patients

Intensive Care Med. 2002 Aug;28(8):1161-3. doi: 10.1007/s00134-002-1389-0. Epub 2002 Jul 5.

Abstract

Objective: CD14, expressed on the cell surface of monocytes and hepatic Kupffer cells, interacts with Gram-positive and Gram-negative bacteria. Upon CD14 stimulation, these cells respond with the enhanced release of cytokines involved in the pathophysiology of sepsis. The purpose of this study was to evaluate whether the genotype distribution of the -260 C-->T promoter polymorphism of the CD14 gene is associated with the development of severe sepsis in trauma patients.

Patients and participants: Fifty-eight severely injured blunt trauma patients with an injury severity score of 16 or more and without pre-existing chronic diseases.

Measurements and results: Genotyping for the single nucleotide exchange polymorphism of the CD14 gene was performed by means of a real-time polymerase chain reaction with fluorescence-labeled hybridization probes. Diagnosis of severe sepsis was based on the criteria of the ACCP/SCCM criteria. Fourteen out of the 58 patients (24.6%) developed a trauma-related severe sepsis. The overall allele frequency was 0.58 for the C allele and 0.42 for the T allele. The genotype distribution (TT 0.19, CT 0.47 and CC 0.35) did not differ significantly from a previously reported control group of healthy blood donors. There was no significant difference of the genotype distribution or allele frequency between trauma patients with severe sepsis and patients with an uncomplicated clinical course.

Conclusions: This pilot study suggests that the CD14 -260 polymorphism is not associated with an increased risk of severe sepsis in trauma patients.

MeSH terms

  • Adult
  • Base Sequence
  • DNA Primers
  • Female
  • Genetic Predisposition to Disease
  • Genotype
  • Humans
  • Lipopolysaccharide Receptors / genetics*
  • Male
  • Middle Aged
  • Pilot Projects
  • Polymorphism, Genetic*
  • Promoter Regions, Genetic*
  • Sepsis / etiology
  • Sepsis / genetics*
  • Wounds, Nonpenetrating / complications*

Substances

  • DNA Primers
  • Lipopolysaccharide Receptors