Undernutrition is a pressing global health problem and undernourished mothers commonly produce offspring who are undernourished. Environmental enteric dysfunction (EED) is a small intestinal (SI) inflammatory enteropathy common in undernourished women. We have tested the hypothesis that the small intestinal (SI) microbiota is an important contributor to EED pathogenesis and that its effects may extend to intrauterine growth restriction, which commonly occurs in undernourished women. To test this hypothesis, we colonized C57BL/6 germ-free mice with bacterial culture collections generated from the SI microbiota of Bangladeshi women who either had a low-BMI (<18.5 kg/m²) with EED (adult small intestinal-low BMI consortia, aSI-L) or a normal BMI (between 18.5 and 30 kg/m²) without EED (adult small intestinal-healthy BMI consortia, aSI-H). Single nucleus RNA-sequencing of deciduas from dams euthanized at embryonic day (E) E11.5, shortly after placentation is complete, demonstrated that tissue-resident uterine NK cells (uNK) that mediate spiral artery remodeling to maximize blood flow and nutrient delivery to the fetus, had some of the highest number of differentially expressed genes (DEGs) between the two groups of colonized animals. These DEGs indicated that aSI-L uNK cells have an increase in overactivation and anti-apoptotic markers and a decrease in IFN-ɣ production. Flow cytometry demonstrated that E11.5 aSI-L deciduas have a decrease in CD27⁺ uNK cells, a marker of lower NK cell production of cytokines such as IFN-ɣ. aSI-L deciduas exhibited lower expression of downstream genes of TGF-β-associated pathways, which help convert cytotoxic, circulating NK cells to non-cytotoxic uNK cells. Immunohistochemical analysis confirmed a reduction TGF-β family members in aSI-L compared to aSI-H deciduas. These results support the notion that the EED-associated SI microbiota affects uNK cell function.