Abstract
The early life period is crucial for the maturation of the intestinal barrier, its immune system, and a life-long beneficial host–microbiota interaction. The study aims to assess the impact of a beneficial dietary (short-chain fructooligosaccharides, scFOS) supplementation vs. a detrimental dietary environment (such as mycotoxin deoxynivalenol, DON) on offspring intestinal immune system developmental profiles. Sows were given scFOS-supplemented or DON-contaminated diets during the last 4 weeks of gestation, whereas force-feeding piglets with DON was performed during the first week of offspring life. Intestinal antigen-presenting cell (APC) subset frequency was analyzed by flow cytometry in the Peyer’s patches and in lamina propria and the responsiveness of intestinal explants to toll-like receptor (TLR) ligands was performed using ELISA and qRT-PCR from post-natal day (PND) 10 until PND90. Perinatal exposure with scFOS did not affect the ontogenesis of APC. While it early induced inflammatory responses in piglets, scFOS further promoted the T regulatory response after TLR activation. Sow and piglet DON contamination decreased CD16+ MHCII+ APC at PND10 in lamina propria associated with IFNγ inflammation and impairment of Treg response. Our study demonstrated that maternal prebiotic supplementation and mycotoxin contamination can modulate the mucosal immune system responsiveness of offspring through different pathways.
Highlights
The early life period is crucial for the maturation of the intestinal barrier, its immune system, and a life-long beneficial host–microbiota interaction
PREB supplementation had a positive impact since PREB sows at D+ 14 and D+ 28 kept quite constant their back fat thickness compared to CTRL sows (* p < 0.05, Figure 2B)
The piglets that were force-fed with Diet. Mycotoxin Contamination (DON) demonstrated a lower growth rate as soon as PND7, resulting in a lower body weight compared to CTRL- and DONgav piglets (p < 0.0001)
Summary
The early life period is crucial for the maturation of the intestinal barrier, its immune system, and a life-long beneficial host–microbiota interaction. The intestinal immune system can be divided into inductive and effector sites. Inductive sites include the gut-associated lymphoid tissues such as Peyer’s patches (PP), isolated lymphoid follicles and the gut-draining mesenteric lymph nodes (MLN). Nutrients 2020, 12, 2115 and the cellular epithelium constitute the main effector sites, harboring large populations of activated. The intestinal antigen-presenting cells (APC), predominantly composed of macrophages and dendritic cells, play a central role in initiating and orchestrating immune responses. At homeostasis, they participate in the tolerance towards dietary components and colonizing commensal microbiota, but they have the ability to fight pathogens [3]
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