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Although Mojibian et al. did not investigate whether the wheat-specific T cell responses correlated with impaired intestinal barrier function, it is reasonable to hypothesise that impaired intestinal barrier function leads to an increased passage of intestinal diabetogenic antigens (e.g. wheat peptides, bacterial agents) that induce the autoimmune cascade typical of type 1 diabetes [ 11, 12, 31].
However, oral administration of ETX produced an increased passage of immunoglobulins from the intestinal lumen to blood in mice and sheep [9] and increased lethal absorption of perfringolysin-O (protein monomer 52 kDa) orally administered to mice [10].
Nevertheless, the current in vitro findings warrant further investigation in vivo because an increased passage of antibiotics may have important implications for both animal and human health.
It was also demonstrated that fumonisin B1 (FB1) affects the membrane composition of IPEC-1 cells resulting in an increased passage of this toxin [ 21].
The hypothesis tested in this study was that an altered integrity of the gut barrier provoked by mycotoxins, could result in an increased passage of antibiotics through the epithelium.
Bacterial infections are an important cause of morbidity and mortality in patients with LC due to an impaired immune function, together with an increased passage of bacteria from the gut (bacterial translocation).
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Leukocytes were captured more efficiently with an increasing passage frequency.
Endothelial dysfunction determines an increase in permeability that is expected to perpetuate intestinal inflammation by allowing increased passage of microbial products and antigenic proteins into the inflamed mucosa.
This likely reflects the increased passage of NO2− and DAF-containing media through the gut with increasing development of the neonates.
Microalbuminuria results from the increased passage of albumin through the glomerular filtration barrier.
Microalbuminuria arises from the increased passage of albumin through the glomerular filtration barrier.
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