1. Maternal dietary exposure to mycotoxin aflatoxin B 1 promotes intestinal immune alterations and microbiota modifications increasing infection susceptibility in mouse offspring.
- Author
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Bastos-Amador P, Duarte EL, Torres J, Caldeira AT, Silva I, Salvador C, Assunção R, Alvito P, and Ferreira M
- Subjects
- Humans, Pregnancy, Mice, Female, Animals, Aflatoxin B1 toxicity, Aflatoxin B1 metabolism, Immunity, Innate, Dietary Exposure, Lactation, Lymphocytes metabolism, Mycotoxins toxicity, Gastrointestinal Microbiome
- Abstract
Mycotoxins are secondary metabolites produced by fungi occurring in food that are toxic to animals and humans. Early-life mycotoxins exposure has been linked to diverse pathologies. However, how maternal exposure to mycotoxins impacts on the intestinal barrier function of progeny has not been explored. Here, exposure of pregnant and lactating C57Bl/6J female mice to aflatoxin B
1 (AFB1 ; 400 μg/kg body weight/day; 3 times a week) in gelatine pellets, from embryonic day (E)11.5 until weaning (postnatal day 21), led to gut immunological changes in progeny. The results showed an overall increase of lymphocyte number in intestine, a reduction of expression of epithelial genes related to microbial defence, as well as a decrease in cytokine production by intestinal type 2 innate lymphoid cells (ILC2). While susceptibility to chemically induced colitis was not worsened, immune alterations were associated with changes in gut microbiota and with a higher vulnerability to infection by the protozoan Eimeria vermiformis at early-life. Together these results show that maternal dietary exposure to AFB1 can dampen intestinal barrier homeostasis in offspring decreasing their capability to tackle intestinal pathogens. These data provide insights to understand AFB1 potential harmfulness in early-life health in the context of intestinal infections., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2023 Elsevier Ltd. All rights reserved.)- Published
- 2023
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