Format

Send to

Choose Destination
Int J Mol Sci. 2014 Nov 7;15(11):20518-37. doi: 10.3390/ijms151120518.

Gliadin peptides as triggers of the proliferative and stress/innate immune response of the celiac small intestinal mucosa.

Author information

1
Department of Translational Medical Science (Section of Pediatrics), University of Naples Federico II, Via S. Pansini 5, Naples 80131, Italy. mv.barone@unina.it.
2
Department of Translational Medical Science (Section of Pediatrics), University of Naples Federico II, Via S. Pansini 5, Naples 80131, Italy. salauric@unina.it.
3
European Laboratory for the Investigation of Food Induced Diseases (ELFID), University of Naples Federico II, Via S. Pansini 5, Naples 80131, Italy. salauric@unina.it.

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.

PMID:
25387079
PMCID:
PMC4264181
DOI:
10.3390/ijms151120518
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Multidisciplinary Digital Publishing Institute (MDPI) Icon for PubMed Central
Loading ...
Support Center