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Captive Primates; Celiac Disease, Gene Expression
The gluten diet is responsible for the symptoms of celiac disease in genetically prone humans. In non-human primates in captivity the feed contains traces of gluten and can trigger systemic inflammatory reactions with clinical signs compatible with celiac disease. Submeter Leontocebus fuscicollis from captivity to periods of gluten diet (GD) and gluten free diet (GFD) to assess the impact of gluten on stool consistency and gene expression of cytokines, β-defensin and Toll like receptor 5 (TLR5) ) it can be verified by blood and real-time PCR evaluation that the animals were responsive to this feeding stimulus. β-defensin expression increased in GD-fed foods. And the expression normalized between 30 and 45 days in GFD. However, a TLR5 gene expression was not affected with a GD. All other genes differentiated (P < 0.05) between the two diet periods. The NEF2, CD83 and HLA-DQB1 genes increased their compliant expressions in the shift from the GFD to GD period, and when reintroduced into the GFD as expressions normalized. However, TNFSF13B completely decreased from the GFD period and continued to decline into the remission period. The HLA-DQA1 gene decreased its expression when completed and reintroduced into the GFD. Regarding the symptom of diarrhea, the stool consistency of those fed a GFD was more common or diarrhea, whereas it was normal in those fed a GD. Extrapolating our results to humans, we conclude that some specific blood cytokines for celiac patients, when altered with DG, can normalize with a reintroduction of GFD, or expressions of its expression, which is quite different from celiac humans that persist in highs or lows expressions for life.