Fetal exposure to chorioamnionitis can impact the outcomes of the developing fetus both at the time of birth, and in the subsequent neonatal period. Infants exposed to chorioamnionitis have a higher incidence of GI pathology, including necrotizing enterocolitis, however that mechanism remains undefined. To simulate the fetal exposure to maternal inflammation (FEMI) induced by chorioamnionitis, pregnant mice (C57Bl/6J, IL-6−/−, RAG−/−, or TNFR1−/−) were injected intraperitoneally on e15.5 with lipopolysaccharide (LPS) 100 µg/kg. Pups were delivered at term, and reared to P0, P7, P14, P28 or P56. Serum and intestinal tissue samples were collected to quantify growth, inflammatory markers, histologic intestinal injury, and goblet and Paneth cells. To determine if FEMI increased subsequent susceptibility to intestinal injury, a secondary dose of LPS (100 µg/kg) was given on P5 prior to tissue harvesting on P7. FEMI had no effect on growth of the offspring or their small intestine. FEMI significantly decreased both goblet and Paneth cells numbers while simultaneously increasing serum levels of IL-1β, IL-10, KC/GRO, TNF, and IL-6. These alterations were IL-6-dependent, and importantly increased susceptibility to LPS-induced intestinal injury later in life. Our data show that FEMI impairs normal intestinal development by decreasing components of innate immunity and simultaneously increasing markers of inflammation. These changes increase susceptibility to intestinal injury later in life and provide novel mechanistic data to potentially explain why preterm infants exposed to chorioamnionitis prior to birth have a higher incidence of NEC and other gastrointestinal disorders.