IL-10 polymorphism associated with decreased risk for mortality after burn injury

J Surg Res. 2010 Nov;164(1):e141-5. doi: 10.1016/j.jss.2010.07.021. Epub 2010 Aug 6.

Abstract

Objective: Evaluation of single nucleotide polymorphisms (SNPs) in the interleukin-10 promoter (-592 and -819) on risk for death after burn injury.

Methods: Association between the IL-10 SNPs and outcome after burn injury was evaluated in a cohort of 265 patients from Parkland Hospital, Dallas, TX with ≥ 15% TBSA burns without non-burn trauma (ISS ≤ 16), traumatic or anoxic brain injury or spinal cord injury, who survived >48 h under an IRB-approved protocol. Clinical data were collected prospectively and genotyping was conducted by TaqMan assay. Whole blood from 31 healthy volunteers was stimulated with LPS (100 ng/mL) to determine the level of IL-10 expression for each allele by enzyme-linked immunosorbent assay (ELISA).

Results: After adjustment for percent total body surface area (TBSA) burned, inhalation injury, age, gender, and race/ethnicity, carriage of ‑592A and/or ‑819T was significantly associated (P = 0.014) with a decreased risk for death (adjusted odds ratio: 0.404; 95% CI: 0.197-0.829). As the candidate SNPs were in complete linkage disequilibrium, it was not possible to distinguish which allele was associated with decreased mortality risk. Age, inhalation injury, and full-thickness burn size were significantly associated with increased risk for death. In the LPS stimulated blood of healthy controls, carriage of the -592A and/or -819T allele demonstrated a trend for decreased levels of IL-10 (P = 0.079).

Conclusion: Carriage of the ‑592A and/or ‑819T allele in the IL-10 promoter appears to reduce the risk for death after burn injury.

Publication types

  • Research Support, N.I.H., Extramural

MeSH terms

  • Adult
  • Burns / genetics*
  • Burns / mortality*
  • Cohort Studies
  • Female
  • Genotype
  • Humans
  • Hypoxia, Brain / mortality
  • Interleukin-10 / genetics*
  • Linkage Disequilibrium
  • Male
  • Middle Aged
  • Polymorphism, Single Nucleotide*
  • Promoter Regions, Genetic / genetics
  • Risk Factors
  • Spinal Cord Injuries / mortality
  • Young Adult

Substances

  • IL10 protein, human
  • Interleukin-10