Affiliations: Neonatal Intensive Care Unit, Mansoura University
Children's Hospital, Mansoura, Egypt | Department of Medical Microbiology and Immunology,
Faculty of Medicine, Mansoura University, Mansoura, Egypt
Note: [] Correspondence: Hesham Abdel-Hady, MD, PhD, Neonatal Intensive
Care Unit, Mansoura University Children's Hospital, Mansoura 35516, Egypt.
Tel.: +2 0105278051; Fax: +2 050 2234092; E-mail: [email protected]
Abstract: 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.
