Genetic polymorphisms of IL-6-174 and IL-10-1082 in full term neonates with late onset blood stream infections
Verantwortlicher Herausgeber dieser Rubrik:
31. März 2009
18. Mai 2009
28. Juli 2015 (online)
Genetically determined variation in the magnitude of inflammatory response may play a role in determining the risk of developing neonatal sepsis, as well as its outcome. To test the hypothesis that interleukin-6 (IL)-6 -174, IL-10 -1082 genetic polymorphisms are associated with the risk of sepsis and clinical outcomes in full-term neonates with blood stream infections (BSIs). A total of 54 full-term neonates with BSIs and 70 matched controls were included in this case/control study. DNA amplification using polymerase chain reaction with sequence-specific primers followed by NIaIII restriction enzyme digestion was done for detection of promoter single nucleotide polymorphism of IL-6 -174 G/C, amplification refractory mutation system-polymerase chain reaction assay was done for IL-10 -1082 G/A polymorphism in blood samples from all infants enrolled in the study. The IL-6 -174 and IL-10-1082 genotypes were not significantly different in neonates with BSIs compared to controls. Whereas, IL-6-174CC and IL-10-1082GG genotypes were associated with increased risk for mortality [Odds ratio (95% confidence intervals): 6.2 (1.3–28.4), P = 0.02 and 25.0 (2.0–74.3), P < 0.01, respectively]. Moreover, IL-6 174CC and IL-10-1082GG genotypes were significantly higher in neonates who required inotropic support and those who developed disseminated intravascular coagulopathy. The IL-6 -174 CC and IL-10 -1082 GG genotypes were associated with increased risk for mortality, need for inotropic support and development of disseminated intravascular coagulopathy in full-term neonates with BSIs. These findings suggest that the genetic composition of the IL-6 and IL-10 promoter areas play a significant role in the pathogenesis of neonatal BSIs.