Genetic polymorphisms of IL-6-174 and IL-10-1082 in full term neonates with late onset blood stream infections
31 March 2009
18 May 2009
28 July 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.