期刊
CELL REPORTS
卷 20, 期 2, 页码 491-504出版社
CELL PRESS
DOI: 10.1016/j.celrep.2017.06.060
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资金
- NIDDK Digestive Disease Core Research Center [NIH P30 DK42086]
- NIDDK [R37 DK47722, T32 DK007074, F31 DK107297]
- GI Research Foundation of Chicago
- David and Ellen Horing Research Fund
Factors affecting the developing neonatal gut microbiome and immune networks may increase the risk of developing complex immune disorders such as inflammatory bowel diseases (IBD). In particular, peripartum antibiotics have been suggested as risk factors for human IBD, although direct evidence is lacking. Therefore, we examined the temporal impact of the commonly used antibiotic cefoperazone on both maternal and offspring microbiota when administered to dams during the peripartum period in the IL-10-deficient murine colitis model. By rigorously controlling for cage, gender, generational, and murine pathobiont confounders, we observed that offspring from cefoperazone-exposed dams develop a persistent gut dysbiosis into adulthood associated with skewing of the host immune system and increased susceptibility to spontaneous and chemically dextran sodium sulfate (DSS)-induced colitis. Thus, early life exposure to antibiotic-induced maternal dysbiosis during a critical developmental window for gut microbial assemblage and immune programming elicits a lasting impact of increased IBD risk on genetically susceptible offspring.
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