Cytokine gene polymorphisms and length of gestation.

摘要: Preterm birth is a major cause of neonatal mortality, morbidity, and long-term disability.1 parturition complex condition etiologic heterogeneity but appears to be stimulated by local inflammatory cytokine response in significant proportion preterm births, particularly extreme births.2, 3 Two proinflammatory cytokines, tumor necrosis factor-α (TNF-α) interleukin-1β (IL-1β), not only mediate the also induce changes key components pathways labor initiation maintenance, including cervical ripening, rupture fetal membranes, uterine contractions. These cytokines production uterotonic prostaglandins, matrix metalloproteinases, oxytocin receptors.4–8 Interleukin-6 (IL-6) has been assigned both antiinflammatory characteristics plays role transition from innate acquired immunity. In context delivery, IL-6 generally considered elevated plasma levels are marker for syndrome.9 Higher maternal tissues or fluids have associated with increased rates delivery.10–14 It hypothesized that polymorphisms modify gene transcription these may alter pregnancy predispose an risk delivery. The concept shortened gestation heritable trait supported fact one strongest factors delivering personal family history delivery.15–18 Previous studies suggested association between at −308 position TNF-α gene, −174 +3954 IL-1β histologic chorioamnionitis, premature disease.19–24 TNF-α−308 minor polymorphism substitution adenine (A) guanine (G) (G>A). cytosine (C) (G>C). IL-1 β thymine (T) (C>T). objective this analysis was estimate what degree, if any, differences single nucleotide (SNPs) affect length