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

Barone MV, Troncone R, Auricchio S - Int J Mol Sci (2014)

Bottom Line: Undigested gliadin peptides induce innate and adaptive T cell-mediated immune responses.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.

View Article: PubMed Central - PubMed

Affiliation: Department of Translational Medical Science (Section of Pediatrics), University of Naples Federico II, Via S. Pansini 5, Naples 80131, Italy. mv.barone@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.

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Celiac cellular phenotype induced by gliadin/P31–43 in control cells and biopsies. Schematic representation of the effects of gliadin peptide P31–43 on cells and biopsies from normal subjects. The main effects were grouped in three sets: structural alterations (actin modifications, cell shape, adhesion and cell migration), signaling/proliferation (NF-κB, pY-Fak, pY-paxillin, pY-ERK) and stress/innate immunity activation. In all cases, there was a quantitative increase in the markers cited, although in the case of actin, the alterations were qualitative. Numbers indicate the bibliographic references.
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ijms-15-20518-f005: Celiac cellular phenotype induced by gliadin/P31–43 in control cells and biopsies. Schematic representation of the effects of gliadin peptide P31–43 on cells and biopsies from normal subjects. The main effects were grouped in three sets: structural alterations (actin modifications, cell shape, adhesion and cell migration), signaling/proliferation (NF-κB, pY-Fak, pY-paxillin, pY-ERK) and stress/innate immunity activation. In all cases, there was a quantitative increase in the markers cited, although in the case of actin, the alterations were qualitative. Numbers indicate the bibliographic references.

Mentions: Several reports in the literature introduced the concept that gliadin may not be safe for non-celiac individuals (Figure 5).


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

Barone MV, Troncone R, Auricchio S - Int J Mol Sci (2014)

Celiac cellular phenotype induced by gliadin/P31–43 in control cells and biopsies. Schematic representation of the effects of gliadin peptide P31–43 on cells and biopsies from normal subjects. The main effects were grouped in three sets: structural alterations (actin modifications, cell shape, adhesion and cell migration), signaling/proliferation (NF-κB, pY-Fak, pY-paxillin, pY-ERK) and stress/innate immunity activation. In all cases, there was a quantitative increase in the markers cited, although in the case of actin, the alterations were qualitative. Numbers indicate the bibliographic references.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4264181&req=5

ijms-15-20518-f005: Celiac cellular phenotype induced by gliadin/P31–43 in control cells and biopsies. Schematic representation of the effects of gliadin peptide P31–43 on cells and biopsies from normal subjects. The main effects were grouped in three sets: structural alterations (actin modifications, cell shape, adhesion and cell migration), signaling/proliferation (NF-κB, pY-Fak, pY-paxillin, pY-ERK) and stress/innate immunity activation. In all cases, there was a quantitative increase in the markers cited, although in the case of actin, the alterations were qualitative. Numbers indicate the bibliographic references.
Mentions: Several reports in the literature introduced the concept that gliadin may not be safe for non-celiac individuals (Figure 5).

Bottom Line: Undigested gliadin peptides induce innate and adaptive T cell-mediated immune responses.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.

View Article: PubMed Central - PubMed

Affiliation: Department of Translational Medical Science (Section of Pediatrics), University of Naples Federico II, Via S. Pansini 5, Naples 80131, Italy. mv.barone@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.

Show MeSH
Related in: MedlinePlus