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Abstract
Celiac disease (CD) is a frequent inflammatory intestinal disease, with a genetic background, caused by gliadin-containing food. Undigested gliadin peptides induce innate and adaptive T cell-mediated immune responses. The major mediator of the stress and innate immune response to gliadin peptides (i.e., peptide 31–43, P31–43) is the cytokine interleukin-15 (IL-15). The role of epithelial growth factor (EGF) as a mediator of enterocyte proliferation and the innate immune response has been described. In this paper, we review the most recent literature on the mechanisms responsible for triggering the up-regulation of these mediators in CD by gliadin peptides. We will discuss the role of P31–43 in enterocyte proliferation, structural changes and the innate immune response in CD mucosa in cooperation with EGF and IL-15, and the mechanism of up-regulation of these mediators related to vesicular trafficking. We will also review the literature that focuses on constitutive alterations of the structure, signalling/proliferation and stress/innate immunity pathways of CD cells. Finally, we will discuss how these pathways can be triggered by gliadin peptide P31–43 in controls, mimicking the celiac cellular phenotype.
Highlights
Ingested food can cause tissue inflammation through different mechanisms
How innate immune response is related to gliadin biological effects on cells and tissues? What is the mechanism generating the stress/innate immune response? What makes the celiac cells susceptible to gliadin peptides effects? Are non-celiacs not susceptible to these effects?
We will try to answer to these questions discussing some recent data from the literature on the effects of gliadin peptides, in particular P31–43, on control and celiac cells and intestinal biopsies, highlighting their relationship with IL-15 and epithelial growth factor (EGF)/EGFR
Summary
Ingested food can cause tissue inflammation through different mechanisms. In the intestine, and in the enterocyte, nutrients are modulators of various cellular functions and may be involved in tissue immune response and inflammation [1]. Gliadin peptides induce alterations of structure (cell shape, actin modifications, increased permeability [19] and vesicular trafficking alterations [17,20]), signaling [17,18] and proliferation [17] and stress/innate immunity activation in several cell lines [21,22,23,24,25,26] (Figure 1). These data suggest that gliadin peptides (i.e., P31–43) can have several different non-T cell mediated effects, both in cell lines and cells and in biopsies from CD patients, that can be grouped into three sets: cell structural changes, including apoptosis, signaling/proliferative effects and stress/innate immunity activation (Figure 2) How these mechanisms of disease are related to the genetics of CD is unclear.
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