Conjugated linoleic acid protects against gliadin-induced depletion of intestinal defenses
Article first published online: 31 AUG 2011
Copyright © 2011 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim
Molecular Nutrition & Food Research
Special Issue: Lipids as Effectors
Supplement: Lipids as Effectors
Volume 55, Issue Supplement 2, pages S248–S256, September 2011
How to Cite
Bergamo, P., Gogliettino, M., Palmieri, G., Cocca, E., Maurano, F., Stefanile, R., Balestrieri, M., Mazzarella, G., David, C. and Rossi, M. (2011), Conjugated linoleic acid protects against gliadin-induced depletion of intestinal defenses. Mol. Nutr. Food Res., 55: S248–S256. doi: 10.1002/mnfr.201100295
- Issue published online: 26 SEP 2011
- Article first published online: 31 AUG 2011
- Manuscript Accepted: 13 JUL 2011
- Manuscript Revised: 1 JUL 2011
- Manuscript Received: 2 MAY 2011
- Conjugated linoleic acid;
- Gluten toxicity;
- Nrf2-mediated defenses;
- Proteasome-acylpeptide hydrolase activity
Scope: The involvement of oxidative stress in gluten-induced toxicity has been evidenced in vitro and in clinical studies but has never been examined in vivo. We recently demonstrated the protective activity of conjugated linoleic acid (CLA), which functions by the activation of nuclear factor erythroid 2-related factor2 (Nrf2), a key transcription factor for the synthesis of antioxidant and detoxifying enzymes (phase 2). Here, we evaluate the involvement of nuclear factor erythroid 2-related factor2 in gliadin-mediated toxicity in human Caco-2 intestinal cells and in gliadin-sensitive human leukocyte antigen-DQ8 transgenic mice (DQ8) and the protective activity of CLA.
Methods and results: Gliadin effects in differentiated Caco-2 cells and in DQ8 mice, fed with a gliadin-containing diet with or without CLA supplementation, were evaluated by combining enzymatic, immunochemical, immunohistochemical, and quantitative real-time PCR (qRT-PCR) assays. Gliadin toxicity was accompanied by downregulation of phase 2 and elevates proteasome-acylpeptide hydrolase activities in vitro and in vivo. Notably, gliadin was unable to generate severe oxidative stress extent or pathological consequences in DQ8 mice intestine comparable to those found in celiac patients and the alterations produced were hampered by CLA.
Conclusion: The beneficial effects of CLA against the depletion of crucial intestinal cytoprotective defenses indicates a novel nutritional approach for the treatment of intestinal disease associated with altered redox homeostasis.