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Developmental 2,3,7,8-tetrachlorodibenzo-p-dioxin exposure of either parent
enhances the risk of necrotizing enterocolitis in neonatal mice.

Authors	Mokshagundam S, Ding T, Rumph JT, Dallas M, Stephens VR, Osteen KG, Bruner-Tran KL
Submitted By	Submitted Externally on 9/28/2020
Status	Published
Journal	Birth defects research, REFERENCES
Year	2020
Date Published	6/1/2020
Volume : Pages	Not Specified : Not Specified
PubMed Reference	32519502
Abstract	Necrotizing enterocolitis (NEC) is a rare, but potentially fatal intestinal inflammatory condition most often arising in premature infants. Infants provided formula are also at greater risk of developing this disease. Although the majority of formula-fed, preterm infants do not develop NEC, up to 30% of infants with the disease do not survive. Thus, identifying additional, currently unrecognized factors, which may predispose a specific infant to NEC development would be a significant clinical advancement. In this regard, we have previously reported that offspring of female or male mice with a history of developmental exposure to the environmental toxicant 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) exhibit altered sensitivity to inflammatory challenges and are frequently born premature. Herein, we examined the possibility that, compared to unexposed mice (F1NONE ), developmental TCDD exposure of either parent (maternal, F1MTCDD , or paternal, F1PTCDD ) would enhance the risk of NEC in offspring (F2TCDD mice) in association with supplemental formula feeding., Beginning on postnatal day 7, all neonates were randomized to maternal milk only or maternal milk with up to 20 supplemental formula feedings. All pups remained with the Dams and were additionally allowed to nurse ad libitum., Formula-fed F2NONE pups rarely developed NEC while this disease was common in formula-fed F2MTCDD and F2PTCDD mice. Unexpectedly, 50% of F2MTCDD pups that were not provided supplemental formula also developed NEC., Our studies provide evidence that a history of parental TCDD exposure enhances the risk of NEC in offspring and suggest exposure to environmental immunotoxicants such as TCDD may also contribute to this inflammatory disease in humans.

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