IL-10, IL-6 and CD14 polymorphisms and sepsis outcome in ventilated very low birth weight infants.
BACKGROUND
Genetic variation in the innate immune system of the host may play a role in determining the risk of developing infection, as well as outcome from infection.


METHODS
Infectious complications were retrospectively determined in 293 (233 African-American (AA), 57 Caucasian and 3 Hispanic) mechanically ventilated very low birth weight (VLBW) infants (<1500 grams at birth) who were genotyped for the IL-6 -174 G/C, IL-10 -1082 G/A and CD14 -260 C/T single nucleotide polymorphisms (SNPs).


RESULTS
The IL-6 -174C allele was associated with an increased incidence of late blood stream infection (BSI) in AA but not Caucasian infants. In AA infants with the C allele the incidence of late BSI was 20/29 (69%) compared to 94/204 (46%) in homozygous GG infants (RR 2.6, 95% CI: 1.1-6.0, p = 0.021). The IL-10 -1082A allele was associated with an increased incidence of late BSI. One or more episodes of late BSI developed in 14 (35%) of 40 infants with the GG genotype, 71 (49%) of 145 infants with the GA genotype and 63 (58%) of 108 infants with the AA genotype (p = 0.036). Infants with the A allele (AA or GA genotypes) had an incidence of late BSI that was 134/253 (53%) compared to 14/40 (35%) in homozygous GG infants (RR 2.1, 95% CI: 1.04-4.19, p = 0.035). The CD14 -260 C/T SNP did not alter the overall risk for BSI in ventilated VLBW infants. Multiple BSI episodes were more common in the TT genotype group (CC: 17%, CT: 11%, TT: 30%, p = 0.022). This effect was due to the strong effect of the TT genotype on the incidence of multiple BSI in AA infants (CC: 15%, CT: 11%, TT: 39%, p = 0.003).


CONCLUSIONS
The IL-6 -174 G/C, IL-10 -1082 G/A and CD14 -260 C/T SNPs may alter risk for BSI in ventilated VLBW infants.
Baier
R John
RJ
Department of Pediatrics, University of Manitoba, WR 116 735 Notre Dame Avenue Winnipeg, Manitoba, R3E 0L8, Canada. rjbaier@exchange.hsc.mb.ca
Loggins
John
J
Yanamandra
Krishna
K
D018949:Antigens, CD1 / Q000235:genetics*; D016022:Case-Control Studies; D005838:Genotype; D006801:Humans; D007113:Immunity, Innate; D007231:Infant, Newborn; D019102:Infant, Very Low Birth Weight; D016753:Interleukin-10 / Q000235:genetics*; D015850:Interleukin-6 / Q000235:genetics*; D020641:Polymorphism, Single Nucleotide; D011379:Prognosis; D012121:Respiration, Artificial; D012189:Retrospective Studies; D018805:Sepsis / Q000209:etiology* / Q000235:genetics* / Q000473:pathology
D018949:Antigens, CD1; D015850:Interleukin-6; D016753:Interleukin-10