title: Analysis of IL-6, IL-10 and IL-17 genetic polymorphisms as risk factors for sepsis development in burned patients.
abstract: Infection risk, sepsis and mortality after severe burn are primarily determined by patient age, burn size, and depth. Whether genetic differences contribute to otherwise unexpected variability in outcomes is unknown. We sought to determine whether there was an association between IL-6, IL-10 and IL-17 polymorphisms with cytokine production and development of sepsis. We evaluated 71 patients with burns ≥15% TBSA and 109 healthy subjects. The genotypes of IL-6 (-174C/G), IL-10 (-819C/T and -1082A/G) and IL-17 (7488T/C) polymorphisms were identified applying polymerase chain reaction protocols. The cytokine levels in serum were determined with enzyme-linked immunoabsorbent assays. Our results demonstrated no significant differences in the genotype frequencies studied between burn patients and healthy subjects. No significant associations were found among IL-6 and IL-17F genotypes and the related cytokine serum levels. Only IL-10 promoter -1082GG genotype was related to an increased IL-10 production in burned patients. In addition, septic subjects bearing -1082G/G genotype have shown the highest and non-septic bearing -1082A/* genotypes the lowest IL-10 serum levels. All together these data seem to indicate that genetically determined individual difference in IL-10 production might influence the susceptibility to septic complications in burned patients and suggest that these markers might be useful in burned patient management.
authors.affiliation: Plastic Surgery and Burns Therapy Operating Unit, ARNAS, Civic Hospital, Palermo, Italy.
authors.forename: A
authors.initials: A
authors.lastname: Accardo Palumbo
authors.forename: G I
authors.initials: GI
authors.lastname: Forte
authors.forename: D
authors.initials: D
authors.lastname: Pileri
authors.forename: L
authors.initials: L
authors.lastname: Vaccarino
authors.forename: F
authors.initials: F
authors.lastname: Conte
authors.forename: L
authors.initials: L
authors.lastname: D'Amelio
authors.forename: M
authors.initials: M
authors.lastname: Palmeri
authors.forename: A
authors.initials: A
authors.lastname: Triolo
authors.forename: N
authors.initials: N
authors.lastname: D'Arpa
authors.forename: L
authors.initials: L
authors.lastname: Scola
authors.forename: G
authors.initials: G
authors.lastname: Misiano
authors.forename: S
authors.initials: S
authors.lastname: Milano
authors.forename: D
authors.initials: D
authors.lastname: Lio
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D002056:Burns / Q000097:blood / Q000150:complications*; D005260:Female; D005838:Genotype; D006801:Humans; D016753:Interleukin-10 / Q000097:blood / Q000235:genetics*; D020381:Interleukin-17 / Q000097:blood / Q000235:genetics*; D015850:Interleukin-6 / Q000097:blood / Q000235:genetics*; D008297:Male; D008875:Middle Aged; D016133:Polymerase Chain Reaction; D011110:Polymorphism, Genetic; D012307:Risk Factors; D018805:Sepsis / Q000235:genetics*; D055815:Young Adult
chemical_list: D020381:Interleukin-17; D015850:Interleukin-6; D016753:Interleukin-10