Gliadin-Rich Diet Worsens Immune and Redox Impairments in Prematurely Aging Mice

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Díaz del Cerro, Estefanía
Cruces, Julia
Ceprián, Noemí
Fuente, Mónica de la

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SDG

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Gliadin is one of the most important fractions of gluten, a glycoprotein closely linked to the development of negative effects on physiological functions and the development of gastrointestinal diseases, such as celiac disease (CD). Research suggests that inadequate stress responses and anxiety states may trigger or at least contribute to the development of these pathological conditions. Peritoneal leukocytes from Prematurely Aging Mice (PAM), which are chronologically adult mice with compromised responses to stress and anxiety, exhibit functional changes when exposed in vitro to gliadin peptides, resembling some immune alterations found also in CD patients. This observation prompted us to investigate the effects of a gliadin-rich diet on immune function and redox state in PAM. In this study, adult female PAM were fed either a gluten-enriched diet (PAMD, 120 g/kg) or a standard diet (PAMC) for four weeks. Immune function parameters in peritoneal, splenic, and thymic leukocytes (phagocytosis, chemotaxis, Natural Killer activity, lymphoproliferation) and redox markers (glutathione reductase, glutathione peroxidase, reduced/oxidized glutathione, xanthine oxidase activity, lipid peroxidation) were evaluated. The results showed that PAMD exhibited more impaired immune function, lower antioxidant enzyme activities, and reduced glutathione concentrations, as well as higher oxidized glutathione and increased xanthine oxidase activity compared to PAMC. These findings suggest that a gliadin-rich diet worsens immune and redox impairments in PAM, resembling some of the alterations previously described in CD, and indicating the potential of this animal for studying gluten-induced immune dysregulation.

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Díaz-Del Cerro, E., Garrido, A., Cruces, J., Ceprián, N., & De La Fuente, M. (2025). Gliadin-rich diet worsens immune and redox impairments in prematurely aging mice. Cells, 14(4), 279. https://doi.org/10.3390/cells14040279

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Attribution-NonCommercial-NoDerivatives 4.0 Internacional

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