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Salvatore Auricchio

Researcher at University of Naples Federico II

Publications -  185
Citations -  7845

Salvatore Auricchio is an academic researcher from University of Naples Federico II. The author has contributed to research in topics: Gliadin & Coeliac disease. The author has an hindex of 49, co-authored 178 publications receiving 7451 citations. Previous affiliations of Salvatore Auricchio include Istituto Superiore di Sanità & University of Salerno.

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Histologic grading of reflux oesophagitis and its relationship with intra-oesophageal and intragastric pH variables

TL;DR: Endoscopy and histology of the oesophagus seem to be the most valuable diagnostic tools in children with symptoms suggesting gastro-oesophageal reflux disease, and the severity of Oesophagitis appears to be related more to the potency of refluxed material than to oesophileal acid exposure.
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Celiac anti-type 2 transglutaminase antibodies induce differential effects in fibroblasts from celiac disease patients and from healthy subjects

TL;DR: Whether anti-TG2 antibodies protect cells from p31–43-induced damage in a CD model consisting of primary dermal fibroblasts is investigated, and it is suggested that the autoimmune response to TG2, which alone may damage the celiac mucosa, also fails in its protective role in celiac cells.
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An innovative approach to measure compliance to a gluten-free diet

TL;DR: The best-known peptide of this group is represented by the A-gliadin peptide 31–43, which is able to induce a stress/innate immune response of the celiac intestine, mainly mediated by IL-15, and a dipeptidyl aminopeptidase, hydrolyzing N-carbobenzoxy-L-prolyl alanine and leucine.
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Zonula occludens toxin (Zot) interferes with the induction of nasal tolerance to gliadin.

TL;DR: In this paper, the ability of Zonula occludens toxin (Zot) to induce a mucosal response to gliadin was demonstrated per serum antibody production.
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Gliadin intake alters the small intestinal mucosa in indomethacin-treated HLA-DQ8 transgenic mice

TL;DR: 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.