title: Innate immunity SNPs are associated with risk for severe sepsis after burn injury.
abstract: OBJECTIVE
  To analyze allelic association with clinical outcome in a cohort of burn patients.
  
  
  METHODS
  Two hundred twenty-eight individuals with burns > or =15% total body surface area without significant non-burn related trauma who survived >48 hours post-admission were enrolled. One hundred fifty-nine of these patients were analyzed previously.
  
  
  METHODS
  Candidate polymorphisms within interleukin-1 beta (IL-1beta), interleukin-6 (IL-6), tumor necrosis factor alpha (TNF-alpha), cellular differentiation marker 14 (CD14) and toll-like receptor 4 (TLR4) were evaluated by logistic regression analysis for association with increased risk for severe sepsis (sepsis plus organ dysfunction or shock).
  
  
  RESULTS
  After adjustment for age, burn size, ethnicity, gender and inhalation injury, alleles at TNF-alpha (308G, p=0.013), TLR4 (+896G, p=0.027), IL-6 (174C, p=0.040) and CD14 (159C, p=0.047) were significantly associated with an increased risk for severe sepsis.
  
  
  CONCLUSIONS
  Carriage of variant alleles at immune response genes were associated with increased risk for severe sepsis after burn injury.
authors.affiliation: University of Texas Southwestern Medical Center, Department of Surgery, Dallas, TX 75390-9160, USA. robert.barber@utsouthwestern.edu
authors.forename: Robert C
authors.initials: RC
authors.lastname: Barber
authors.forename: Ling-Yu E
authors.initials: LY
authors.lastname: Chang
authors.forename: Brett D
authors.initials: BD
authors.lastname: Arnoldo
authors.forename: Gary F
authors.initials: GF
authors.lastname: Purdue
authors.forename: John L
authors.initials: JL
authors.lastname: Hunt
authors.forename: Jureta W
authors.initials: JW
authors.lastname: Horton
authors.forename: Corinne C
authors.initials: CC
authors.lastname: Aragaki
mesh_terms: D000328:Adult; D000483:Alleles; D002056:Burns / Q000150:complications / Q000235:genetics*; D005260:Female; D020022:Genetic Predisposition to Disease; D006801:Humans; D007113:Immunity, Innate / Q000235:genetics*; D053583:Interleukin-1beta / Q000235:genetics; D015850:Interleukin-6 / Q000235:genetics; D018950:Lipopolysaccharide Receptors / Q000235:genetics; D008297:Male; D008875:Middle Aged; D020641:Polymorphism, Single Nucleotide; D012189:Retrospective Studies; D012307:Risk Factors; D018805:Sepsis / Q000209:etiology / Q000235:genetics*; D012720:Severity of Illness Index; D051197:Toll-Like Receptor 4 / Q000235:genetics; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics
chemical_list: D053583:Interleukin-1beta; D015850:Interleukin-6; D018950:Lipopolysaccharide Receptors; C495345:TLR4 protein, human; D051197:Toll-Like Receptor 4; D014409:Tumor Necrosis Factor-alpha