Celiac disease (CD), a common heritable chronic inflammatory condition of the small intestine caused by permanent intolerance to gluten/gliadin (prolamin), is characterized by a complex interplay between genetic and environmental factors [1
]. The prolamin fractions in cereal grains (gliadin in wheat and similar alcohol-soluble proteins in other cereals, secalin in rye, hordein in barley) are the environmental stimuli responsible for the development of intestinal damage associated with CD [2
]. The classical presentation of CD as a pediatric predominant disorder, is characterized by small-intestinal villous atrophy and crypt hyperplasia [4
]. However especially in adult-onset patients, a preserved mucosal architecture characterized by dense lymphocytic infiltration, with no villous atrophy or crypt hyperplasia can also be observed.
An interplay between innate and adaptive immune responses to ingested gluten [5
] is involved in CD. Developments in proteomics have provided an important contribution to the understanding of the biochemical and immunological aspects and the mechanisms involved in the toxicity of prolamins [7
]. It has been demonstrated that the gliadin sequence contains regions which play a special role in CD pathogenesis: exert a cytotoxic activity or immunomodulatory activity. Other regions trigger oxidative stress and induce the release of pro-inflammatory cytokines [8
]. As a consequence, elimination of gluten from the diet (gluten free diet, GDF) results in a clinical improvement in CD patients.
A previous celiac disease genome-wide association study (GWAS) demonstrated risk variants in the human leukocytes antigen (HLA) region [10
]. HLA-DQ2 and HLA-DQ8 risk alleles are necessary, but not sufficient, for celiac disease development. Recent studies have shown that 6% of the European and USA population do not present these alleles [12
]. Therefore other no-HLA risk genes need to be investigated.
Several dietary components exert anti-inflammatory and antioxidant roles and have a protective effect on intestinal epithelium [14
], therefore their adoption could contribute to preserving intestinal barrier integrity and play a protective role against the toxicity of gliadin peptides in CD subjects [15
]. In recent years, the creation of the two research fields “Nutrigenomics” and “Nutrigenetics”, has enabled the elucidation of some interactions between diet, nutrients and genes. “Nutrigenetics” refers to genetically determined differences in reactivity of individuals to specific foods, while “Nutrigenomics” refers to the functional interactions of food with the genome. The aim of the review is to summarize the approach of “Omic” sciences to elucidate the complex relationships between dietary factors, genetic polymorphisms and the gut structure as well as the functions in celiac disease.