Gestational vitamin A deficiency reduces the intestinal immune response by decreasing the number of immune cells in rat offspring

Vitamin A (VA) is a critical micronutrient for life, especially during growth and development. There is a close relationship between VA deficiency (VAD) and the morbidity of diarrhea in the clinical setting. However, the regulatory mechanisms of VA are not clearly understood. Specific-pathogen–free Wistar rats received a diet with or without VA before gestation. The offspring were submitted to an abdominal injection of Escherichia coli lipopolysaccharide. After the challenge, which lasted for 12 h, the serum retinol was detected by high-performance liquid chromatography, and the level of immunoglobulin A in the stool was analyzed by enzyme-linked immunosorbent assay. The lymphocyte immunophenotypes were evaluated with the use of flow cytometry with samples collected from the spleen, the mesenteric lymph nodes, Peyer patches, and intestinal intraepithelial lymphocytes. Early life VAD, independent of the lipopolysaccharide challenge, significantly decreased serum retinol level and CD8+ intestinal intraepithelial lymphocytes. The level of immunoglobulin A secretion and percentages of splenic CD4+CD8+ T cells were affected by the interaction effects of the lipopolysaccharide challenge and VAD treatment. Gestational VAD significantly increased the percentages of B cells in the mesenteric lymph nodes and decreased the percentages of CD11 C+ dendritic cells and CD4+CD25+ T cells from the Peyer patches. The lipopolysaccharide challenge only significantly increased percentages of splenic CD4+CD25+ T cells. The intestinal tissue of the pups with VAD displayed mild inflammation. Gestational or early life VAD decreases the numbers of immune cells in offspring, which may partly suppress the activities of the mucosal immune responses in the intestine. This suggests that more attention should be given to the VA nutritional state of children and women of reproductive age.