http://www.cnr.it/ontology/cnr/individuo/prodotto/ID294637

Gliadin intake alters the small intestinal mucosa in indomethacin-treated HLA-DQ8 transgenic mice (Articolo in rivista)

Type

Articolo in rivista (Classe)
Prodotto della ricerca (Classe)

Label

Gliadin intake alters the small intestinal mucosa in indomethacin-treated HLA-DQ8 transgenic mice (Articolo in rivista) (literal)

Anno

2014-01-01T00:00:00+01:00 (literal)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#doi

10.1152/ajpgi.00002.2014 (literal)

Alternative label

Mazzarella G.; Bergamo P.; Maurano F.; Luongo D.; Rotondi Aufiero V.; Bozzella G.; Palmieri G.; Troncone R.; Auricchio S.; David C.; Rossi M. (2014)
Gliadin intake alters the small intestinal mucosa in indomethacin-treated HLA-DQ8 transgenic mice
in American journal of physiology: Gastrointestinal and liver physiology
(literal)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori

Mazzarella G.; Bergamo P.; Maurano F.; Luongo D.; Rotondi Aufiero V.; Bozzella G.; Palmieri G.; Troncone R.; Auricchio S.; David C.; Rossi M. (literal)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#url

http://www.scopus.com/inward/record.url?eid=2-s2.0-84905272141&partnerID=q2rCbXpz (literal)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroVolume

307 (literal)

Rivista

American journal of physiology: Gastrointestinal and liver physiology (Rivista)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroFascicolo

3 (literal)

Note

Scopu (literal)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#affiliazioni

Institute of Food Sciences, National Research Council, Avellino, Italy; Institute of Protein Biochemistry, National Research Council, Naples, Italy; European Laboratory for Investigation of Food Induced Diseases and Department of Pediatrics, University 'Federico II' of Naples, Naples, Italy; Department of Immunology, Mayo Clinic College of Medicine, Rochester, MN, United States (literal)

Titolo

Gliadin intake alters the small intestinal mucosa in indomethacin-treated HLA-DQ8 transgenic mice (literal)

Abstract

Celiac disease (CD) is an enteropathy caused by the ingestion of wheat gluten in genetically susceptible individuals. A complete understanding of the pathogenic mechanisms in CD has been hindered because of the lack of adequate in vivo models. In the present study, we explored the events after the intragastric administration of gliadin and of the albumin/ globulin fraction from wheat in human leukocyte antigen-DQ8 transgenic mice (DQ8 mice) treated with indomethacin, an inhibitor of cyclooxygenases (COXs). After 10 days of treatment, mice showed a significant reduction of villus height, increased crypt depth, increased number of lamina propria-activated macrophages, and high basal interferon-? secretion in mesenteric lymph nodes, all of which were specifically related to gliadin intake, whereas the albumin/globulin fraction of wheat was unable to induce similar changes. Cotreatment with NS-398, a specific inhibitor of COX-2, also induced the intestinal lesion. Enteropathy onset was further characterized by high levels of oxidative stress markers, similar to CD. Biochemical assessment of the small intestine revealed the specific activation of matrix metalloproteinases 2 and 9, high caspase-3 activity, and a significant increase of tissue transglutaminase protein levels associated with the intestinal lesion. Notably, after 30 days of treatment, enteropathic mice developed serum antibodies toward gliadin (IgA) and tissue transglutaminase (IgG). We concluded that gliadin intake in combination with COX inhibition caused a basal inflammatory status and an oxidative stress condition in the small intestine of DQ8 mice, thus triggering the mucosal lesion and, subsequently, an antigen-specific immunity. © 2014 the American Physiological Society. (literal)

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