Nutrigenomics applied to an animal model of Inflammatory Bowel Diseases: Transcriptomic analysis of the effects of eicosapentaenoic acid- and arachidonic acid-enriched diets

Abstract

Nutrigenomics applied to an animal model of Inflammatory Bowel Diseases: Transcriptomic analysis of the effects of eicosapentaenoic acidand arachidonic acid-enriched diets AbstractIn vivo models of Inflammatory Bowel Diseases (IBD) elucidate important mechanisms of chronic inflammation. Complex intestinal responses to food components create a unique "fingerprint" discriminating health from disease. Five-week-old IL10−/− and C57BL/6J (C57; control) mice were inoculated orally with complex intestinal microflora (CIF) and/or pure cultures of Enterococcus faecalis and E. faecalis (EF) aiming for more consistent inflammation of the intestinal mucosa. Inoculation treatments were compared to noninoculated IL10−/− and C57 mice, either kept in specific pathogen free (SPF) or conventional conditions (2×5 factorial design). At 12 weeks of age, mice were sacrificed for intestinal histological (HIS) and transcriptomic analysis using limma and Ingenuity Pathway Analysis Software. Colonic HIS was significantly affected (P < 0.05) in inoculated IL10−/− mice and accounted for approximately 60% of total intestinal HIS. Inoculation showed a strong effect on colonic gene expression, with more than 2000 genes differentially expressed in EF·CIF-inoculated IL10−/− mice. Immune response gene expression was altered (P < 0.05) in these mice. The second study investigated the effect of arachidonic (AA) and eicosapentaenoic acid (EPA) on colonic HIS and gene expression to test whether EPA, contrary to AA, diminished intestinal inflammation in EF·CIF IL10−/− mice (2×4 factorial design). AIN-76A (5% corn oil) and AIN-76A (fat-free) +1% corn oil supplemented with either 3.7% oleic acid (OA), AA or EPA were used. IL10−/− mice fed EPA-and AAenriched diets had at least 40% lower colonic HIS (P < 0.05) than those fed control diets (AIN-76A and OA diets). The expression of immune response and 'inflammatory disease' genes (down-regulated: TNF, IL6, S100A8, FGF7, PTGS2; up-regulated: PPAR, MGLL, MYLK, PPSS23, ABCB4 with EPA and/or AA) was affected in IL10−/−mice fed EPA-and AA-enriched diets, compared to those fed AIN-76A diet. AbstractIn vivo models of Inflammatory Bowel Diseases (IBD) elucidate important mechanisms of chronic inflammation. Complex intestinal responses to food components create a unique "fingerprint" discriminating health from disease. Five-week-old IL10 −/− and C57BL/6J (C57; control) mice were inoculated orally with complex intestinal microflora (CIF) and/or pure cultures of Enterococcus faecalis and E. faecalis (EF) aiming for more consistent inflammation of the intestinal mucosa. Inoculation treatments were compared to non-inoculated IL10 −/− and C57 mice, either kept in specific pathogen free (SPF) or conventional conditions (2 × 5 factorial design). At 12 weeks of age, mice were sacrificed for intestinal histological (HIS) and transcriptomic analysis using limma and Ingenuity Pathway Analysis Software. Colonic HIS was significantly affected (P < 0.05) in inoculated IL10 −/− mice and accounted for approximately 60% of total ...

The Effects of n-3 Polyunsaturated Fatty Acid-Rich Salmon on Inflammatory Bowel Diseases

“…For example, curcumin (a polyphenolic compound found in some foods such as the spice turmeric), reduced histological signs of colonic inflammation and the expression levels of genes in pro-inflammatory pathways in a mouse model of IBD ). The influences of dietary PUFA supplementation on mice with chronic colitis were studied by Knoch et al (2009;2010a) and Roy et al (2007). The results of these experiments showed mild anti-inflammatory effects for both n-3 and n-6 PUFA, the former via the activation of a PPAR transcription factor.…”

“…However, single nutrients may exert different protective effects than whole foods which provide these components. Possible antiinflammatory features of extracted long-chain n-3 PUFA (Calder, 2009;Knoch et al, 2009;Knoch et al, 2010a;Roy et al, 2007) may function differently when in a food matrix (KrisEtherton & Hill, 2008). Dietary n-3 PUFA can be ingested as highly purified extracts of single n-3 PUFA, fish oil (mixture of PUFA) or marine fish (nutrient package and rich in n-3 PUFA).…”

Study of the effects of dietary polyunsaturated fatty acids: Molecular mechanisms involved in intestinal inflammation

“…Genetic mouse models with certain gene mutations and deficiencies such as the interleukin 10 gene deficient (IL10 -/-) mouse (Kühn et al, 1993;Roy et al, 2007) and the multidrug resistance gene deficient (mdr1a -/-) mouse show chronic and spontaneous intestinal inflammation. Some of these models which are commercially available have a single gene defect to induce a human IBD-like colitis.…”

Essential amino acid usage and evolutionary nutrigenomics of eukaryotes - insights into the differential usage of amino acids in protein domains and extra-domains

“…Most of these dozens of papers in the nutrigenomics field are still theoretical, proposing possible experimental strategies and future perspectives to study interactions between genomics and nutrition (Peregrin, 2001;van Ommen and Stierum, 2002;Chavez and Munoz, 2003;Muller and Kersten, 2003;Trayhurn, 2003;Chadwick, 2004). Researchers agree that nutrigenomics shall be considered the study of both the genetic factors influencing organisms' response to diet (Low and Tai, 2007) and the effects of food on the host genome and gene expression (Ozdemir and Godard, 2007;Roy et al, 2007;Ye et al, 2007). Like pharmacogenomics when thinking about drugs, nutrigenomics shall be used in the near future to predict the very best relationship between the genome and particular nutrients, trying to measure the amounts and different kinds of nutrients that would be preferred for a given individual in order that his/her metabolism work as well as possible (Fenech, 2005;Afman and Muller, 2006;Ghosh et al, 2007).…”

“…Thus, nutrigenomics raises similar ethical, legal and social issues as does pharmacogenomics, particularly in regard to how the public will access nutrigenetic tests and associated nutritional advice (Castle and Ries, 2007;Ozdemir and Godard, 2007). Current approaches in nutrigenomics have addressed a number of interesting topics in biology, such as: cancer research (Davis and Milner, 2004;Junien and Gallou, 2004;Davis, 2007;Martin, 2007), longevity (Ye et al, 2007), obesity (Palou et al, 2004), inflammation (Roy et al, 2007), cardiovascular disease (Davis, 2007;Low and Tai, 2007), eye health (Delcourt, 2007), fertility (Dawson, 2006), and the study of taste and food preferences (El-Sohemy et al, 2007). It is noteworthy that no one has yet tried to understand how diet has been influencing genome modification of organisms over time, and therefore, the present study attempts to take this evolutionary perspective into account.…”