Phytochemicals and Celiac disease

Celiac disease is defined as a condition of damaging the lining of the small intestine as a result of an autoimmune disorder of the small intestine resulting in some food parts not being absorbed. Some researchers indicated the sequence of alpha-gliadin (amino acids 31-49) is one of the triggers of the immune system in celiac spruewas because if its toxicity (1)

Types of foods to prevent and treat Celiac disease
1. Quinoa
Quinoa is a highly nutritive plant from the Andes, with low concentrations of prolamins, that has been recommended as part of a gluten-free diet; however, few experimental data support this recommendation. In the study of Variable activation of immune response by quinoa (Chenopodium quinoa Willd.) prolamins in celiac disease, researchers at the King's College London, indicated that Most quinoa cultivars do not possess quantifiable amounts of celiac-toxic epitopes. However, 2 cultivars had celiac-toxic epitopes that could activate the adaptive and innate immune responses in some patients with celiac disease. These findings require further investigation in the form of in vivo studies, because quinoa is an important source of nutrients for patients with celiac disease(2).

2.  Red berries and kiwi
Ascorbate (vitamin C) found abundantly in red beries and kiwi is known to show the inhibited effects on NF-κB which has an important role in coeliac disease (CD. The addition of ascorbate to in vitro culture gliadin-challenged biopsies blocked the secretion of nitrites (p=0.013), IFNγ (p=0.0207), TNFα (p=0.0099), IFNα (p=0.0375), and IL-6 (p=0.0036) compared to samples from non-ascorbate supplemented culture. Cytokine secretion was downregulated by ascorbate even to lower values than those observed in basal cultures (IFNγ: p=0.0312; TNFα: p=0.0312; IFNα: p=0.0312; and IL-6: p=0.0078). Gliadin-challenge induced IL-15 production in biopsies from treated CD patients, while the addition of ascorbate to culture medium completely inhibited IL-15 production. Moreover, the inhibition of IL-15 by ascorbate took place even in the only treated CD-patient who had basal IL-15 production(3).

3. Olive oil
In the study of  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, researchers at the Consiglio Nazionale delle Ricerche (CNR-ISA, showed that 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(4).

4.  Blueberries, cherries and blackberries (quercetin), Tomato (lycopene) and  olive oil (tyrosol)
. In the study of  the effect of the lycopene, quercetin and tyrosol natural antioxidants on the inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) gene expression in RAW 264.7 macrophages stimulated by gliadin in association with IFN-gamma, found that the IFN-gamma plus gliadin combination treatment was capable of enhancing iNOS and COX-2 gene expression and nuclear factor-kappaB (NF-kappaB), interferon regulatory factor-1 (IRF-1) and signal transducer and activator of transcription-1alpha (STAT-1alpha) activation induced by reactive oxygen species generation at 24 h. Lycopene, quercetin and tyrosol inhibited all these effects. The results here reported suggest that these compounds may represent non toxic agents for the control of pro-inflammatory genes involved in celiac disease(5)

6. Etc.

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Sources
(1) http://www.ncbi.nlm.nih.gov/pubmed/7984348
(2) http://www.ncbi.nlm.nih.gov/pubmed/22760575
(3) http://www.ncbi.nlm.nih.gov/pubmed/21420224
(4) http://www.ncbi.nlm.nih.gov/pubmed/21954188
(5) http://www.ncbi.nlm.nih.gov/pubmed/17477920