Literature DB >> 33707054

The gliadin p31-43 peptide: Inducer of multiple proinflammatory effects.

Fernando Gabriel Chirdo1, Salvatore Auricchio2, Riccardo Troncone3, Maria Vittoria Barone3.   

Abstract

Coeliac disease (CD) is the prototype of an inflammatory chronic disease induced by food. In this context, gliadin p31-43 peptide comes into the spotlight as an important player of the inflammatory/innate immune response to gliadin in CD. The p31-43 peptide is part of the p31-55 peptide from α-gliadins that remains undigested for a long time, and can be present in the small intestine after ingestion of a gluten-containing diet. Different biophysical methods and molecular dynamic simulations have shown that p31-43 spontaneously forms oligomeric nanostructures, whereas experimental approaches using in vitro assays, mouse models, and human duodenal tissues have shown that p31-43 is able to induce different forms of cellular stress by driving multiple inflammatory pathways. Increased proliferative activity of the epithelial cells in the crypts, enterocyte stress, activation of TG2, induction of Ca2+, IL-15, and NFκB signaling, inhibition of CFTR, alteration of vesicular trafficking, and activation of the inflammasome platform are some of the biological effects of p31-43, which, in the presence of appropriate genetic susceptibility and environmental factors, may act together to drive CD.
© 2021 Elsevier Inc. All rights reserved.

Entities:  

Keywords:  Celiac disease; Inflammation; Innate immunity; Small intestine; p31–43

Mesh:

Substances:

Year:  2020        PMID: 33707054     DOI: 10.1016/bs.ircmb.2020.10.003

Source DB:  PubMed          Journal:  Int Rev Cell Mol Biol        ISSN: 1937-6448            Impact factor:   6.813


  6 in total

1.  Gliadin Peptide P31-43 Induces mTOR/NFkβ Activation and Reduces Autophagy: The Role of Lactobacillus paracasei CBA L74 Postbiotc.

Authors:  Mariangela Conte; Federica Nigro; Monia Porpora; Claudia Bellomo; Francesca Furone; Andrea Luigi Budelli; Roberto Nigro; Maria Vittoria Barone; Merlin Nanayakkara
Journal:  Int J Mol Sci       Date:  2022-03-26       Impact factor: 5.923

2.  Inflammation Is Present, Persistent and More Sensitive to Proinflammatory Triggers in Celiac Disease Enterocytes.

Authors:  Monia Porpora; Mariangela Conte; Giuliana Lania; Claudia Bellomo; Luciano Rapacciuolo; Fernando Gabriel Chirdo; Renata Auricchio; Riccardo Troncone; Salvatore Auricchio; Maria Vittoria Barone; Merlin Nanayakkara
Journal:  Int J Mol Sci       Date:  2022-02-10       Impact factor: 5.923

Review 3.  Pivotal Role of Inflammation in Celiac Disease.

Authors:  Maria Vittoria Barone; Renata Auricchio; Merlin Nanayakkara; Luigi Greco; Riccardo Troncone; Salvatore Auricchio
Journal:  Int J Mol Sci       Date:  2022-06-28       Impact factor: 6.208

Review 4.  Type 2 Transglutaminase in Coeliac Disease: A Key Player in Pathogenesis, Diagnosis and Therapy.

Authors:  Gaetana Paolella; Silvia Sposito; Antonio Massimiliano Romanelli; Ivana Caputo
Journal:  Int J Mol Sci       Date:  2022-07-06       Impact factor: 6.208

Review 5.  Interplay Between Gluten, HLA, Innate and Adaptive Immunity Orchestrates the Development of Coeliac Disease.

Authors:  Jordan Voisine; Valérie Abadie
Journal:  Front Immunol       Date:  2021-06-02       Impact factor: 7.561

Review 6.  Programmed Cell Death in the Small Intestine: Implications for the Pathogenesis of Celiac Disease.

Authors:  Federico Perez; Carolina Nayme Ruera; Emanuel Miculan; Paula Carasi; Fernando Gabriel Chirdo
Journal:  Int J Mol Sci       Date:  2021-07-10       Impact factor: 5.923

  6 in total

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