Gynécologie & Obstétrique

Gynécologie & Obstétrique
Libre accès

ISSN: 2161-0932


Association of mRNA Expression of Interleukin-6 and Interleukin-10 with Organochlorine Pesticides in Idiopathic Preterm Birth

Deepika Nayan*, Suman S, Guleria K, Suneja A, Sharma T, Banerjee BD

Objectives: India is one of the nation’s leading in number of Preterm Births (PTB), as reported by WHO. Despite extensive research the exact cause of PTB remains elusive. The present study was designed to gain insight into inflammatory genes (proinflammatory IL-6 and anti inflammatory IL-10) and environment (Organochlorine Pesticides-OCPs) interaction in etiopathogenesis of PTB.

Methods: Maternal blood and placental tissue samples of PTB cases (n=263) and equal number of term delivery controls (n=263) were collected at the time of delivery. mRNA expression of IL-6 and IL-10 gene was analysed using real-time PCR and OCP levels by gas chromatography.

Results: mRNA expression of IL-6 gene (pro inflammatory) was 11.73 folds high in maternal blood and 2.60 folds higher in placental tissue in PTB compared to term birth cases. mRNA expression of IL-10 gene (anti inflammatory) was 25 folds lower in maternal blood and 10 folds lower in placental tissue of PTB compared to term deliveries. Significant association was found between the higher levels of Beta Hexachlorocyclohexane (β HCH) and ortho, Para Dichlorodiphenyldichloroethane (o’p’-DDD) in maternal blood with PTB (OR 1.27 and 5.45 respectively). Also, significant association was found between higher levels of para, para Dichlorodiphenyl Dichloroethylene (p’p’-DDE) in placental tissue with PTB (OR 1.16). Interaction between IL-6 and high levels of β-HCH, dieldrin and DD resulted in significant reduction in Period of Gestation (POG) by 7-12 days and interaction between IL-10 and β-HCH by 12 days.

Conclusion: The gene (IL) environment (OCPs) interaction resulted in significant reduction of POG ranging from 1-2 weeks. Thus, the present study identified the gene environment interaction as a potential risk for PTB and emerges as a molecular tool in etiopathogesis of PTB.