1. The murine enterocyte cell line Mode-K is a novel and reliable in vitro model for studies on gluten toxicity.
- Author
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Luongo D, Treppiccione L, Maurano F, Rossi M, and Bergamo P
- Subjects
- Animals, Caco-2 Cells, Cell Differentiation, Cell Line, Duodenum drug effects, Enterocytes cytology, Gliadin toxicity, Humans, In Vitro Techniques, Mice, Models, Biological, Triticum chemistry, Enterocytes drug effects, Glutens toxicity
- Abstract
The resemblance of physiological traits of cell lines with their target/original tissue is an important prerequisite for the choice of the in vitro model. Although cytoprotective defenses, activated by the nuclear factor erythroid 2-related factor2 (Nrf2), have a preeminent importance in intestinal protection, nevertheless their levels inin vitro models have been never compared with those of their original tissue. Basal level of Nrf2-mediated defenses in murine enterocyte cells (Mode-K) and in human colon adenocarcinoma cells -at differentiated (DCaco2) or confluent stage (CCaco2)- were compared with those found in mouse or human duodenum. The pro-oxidant and cytotoxic effects of peptic-tryptic digest of gluten prepared from wheat bread (PT-b), einkorn (PT-e) or durum wheat (PT-d) were evaluated in Mode-k and DCaco2 by combining enzymatic, immune-enzymatic and real-time PCR assay. The results presented reveal that Mode-k cells resemble cytoprotective defenses of human/murine duodenum and are more susceptible to pro-oxidant, cytotoxic and pro-inflammatory effect of gliadin digest (in comparison with Caco2). Prolamins digests from the considered wheat exhibit different inhibitory effect on Nrf2-mediated defenses (PT-b > PT-e > PT-d). These data indicate, for the first time, that Mode-k are a reliable model for investigating wheat prolamins toxicity and for evaluating the signaling pathway of gluten-associated disease., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2020 Elsevier Ltd. All rights reserved.)
- Published
- 2020
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