Developmental 2,3,7,8-tetrachlorodibenzo-p-dioxin exposure of either parent enhances the risk of necrotizing enterocolitis in neonatal mice.
dioxin
ileum
lung
multigenerational
necrotizing enterocolitis
Journal
Birth defects research
ISSN: 2472-1727
Titre abrégé: Birth Defects Res
Pays: United States
ID NLM: 101701004
Informations de publication
Date de publication:
10 2020
10 2020
Historique:
received:
19
12
2019
revised:
22
04
2020
accepted:
20
05
2020
pubmed:
11
6
2020
medline:
19
8
2021
entrez:
11
6
2020
Statut:
ppublish
Résumé
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 (F1 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 F2 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.
Sections du résumé
BACKGROUND
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 (F1
METHODS
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.
RESULTS
Formula-fed F2
CONCLUSIONS
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.
Identifiants
pubmed: 32519502
doi: 10.1002/bdr2.1742
pmc: PMC8274937
mid: NIHMS1712855
doi:
Substances chimiques
Polychlorinated Dibenzodioxins
0
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, U.S. Gov't, Non-P.H.S.
Langues
eng
Sous-ensembles de citation
IM
Pagination
1209-1223Subventions
Organisme : NCI/NIH Cancer Center Support
ID : 5P30 CA68485-19
Organisme : NIH HHS
ID : S10 OD023475
Pays : United States
Organisme : Vanderbilt Mouse Metabolic Phenotyping Center
ID : 2 U24 DK059637-16
Organisme : BLRD VA
ID : I01 BX002853
Pays : United States
Organisme : Research Training Initiative for Student Enhancement
ID : 5R25GM059994
Organisme : NIEHS NIH HHS
ID : T32 ES007028
Pays : United States
Organisme : NIGMS NIH HHS
ID : R25 GM059994
Pays : United States
Organisme : Veterans Administration
ID : I01BX002583
Organisme : NIDDK NIH HHS
ID : U24 DK059637
Pays : United States
Organisme : BLRD VA
ID : IK2 BX002583
Pays : United States
Organisme : NCI NIH HHS
ID : P30 CA068485
Pays : United States
Informations de copyright
© 2020 Wiley Periodicals, Inc.
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