Anti-inflammatory effects of enteral diet components on Crohn's disease-affected tissues in vitro

Meister, Doris; Bode, John; Shand, Alan G.; Ghosh, Subrata

doi:10.1016/s1590-8658(02)80041-x

Cited by 62 publications

(50 citation statements)

References 28 publications

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“…An alternative approach to management of IBD, particularly CD, is EEN. EEN is effective in reducing mucosal cytokine levels, resolving mucosal histological changes and pro-inflammatory-induced gut barrier dysfunction along with reduction in bacterial load (de Jong et al 2007;Leach et al 2008;Meister et al 2002;Nahidi et al 2012Nahidi et al , 2013). The precise mechanism by which EEN suppresses inflammation is unknown; however, it has previously been hypothesised that EEN's therapeutic activity can be attributed to gut rest and/or modulation of gut microbiota.…”

Section: Discussionmentioning

confidence: 99%

The major pathway by which polymeric formula reduces inflammation in intestinal epithelial cells: a microarray-based analysis

et al. 2015

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Nutritional therapy is well established as a means to induce remission in active Crohn's disease (CD). Evidence indicates that exclusive enteral nutrition (EEN) therapy for CD both alters the intestinal microbiota and directly suppresses the inflammatory response in the intestinal mucosa. However, the pathway(s) through which EEN suppresses inflammation is still unknown. Therefore, the aim of the current study was to use microarray technology to investigate the major pathway by which polymeric formula (PF) alters inflammatory processes in epithelial cells in vitro. HT-29 cells were grown to confluence and then co-cultured with tumour necrosis factor (TNF)-a (100 ng/ml) for 5 h in the presence or absence of PF, as used for EEN. Following incubation, RNA was extracted and subjected to polymerase chain reaction (PCR) and microarray analysis. Enzyme-linked immunosorbent assays were employed to evaluate cytokine protein levels. Neither TNF-a nor PF had a toxic effect on cells over the experimental period. Microarray analysis showed that PF modulated the expression of genes specifically linked to nuclear factor (NF)-jB, resulting in downregulation of a number of genes in this pathway. These findings were further confirmed by real-time PCR of selected dysregulated genes as well as reduced expression of IL-6 and IL-8 proteins following PF treatment. The results arising from this study provide evidence that PF alters the inflammatory responses in intestinal epithelial cells through modulation of the NF-jB pathway.

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Section: Discussionmentioning

confidence: 99%

The major pathway by which polymeric formula reduces inflammation in intestinal epithelial cells: a microarray-based analysis

et al. 2015

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“…Cytokines produced in, and released from, the inflamed mucosa in active CD are also known to enhance bone resorption and subsequent bone loss [37]. Therefore, as EEN has been shown to reduce inflammation, [21,38,39] this nutritional therapy may normalize bone turnover through a reduction in inflammation. Certainly, the concurrent fall in inflammatory scores with EEN therapy in the present study supports this supposition, as does the correlation of BAP (but not CTX) with inflammatory markers.…”

Section: Discussionmentioning

confidence: 99%

Effect of exclusive enteral nutrition on bone turnover in children with Crohn’s disease

et al. 2009

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“…Several studies have shown the efficacy of dietary fish oil (FO) consumption in IBD (6)(7)(8)(9)(10). Long-chain omega-3 polyunsaturated fatty acids (PUFA), such as docosahexaenoic acid (DHA) and ecosapentaenoic acid (EPA), modulate inflammatory responses through several mechanisms.…”

Section: Introductionmentioning

confidence: 99%

Dietary Fish Oil Alters T Lymphocyte Cell Populations and Exacerbates Disease in a Mouse Model of Inflammatory Colitis

et al. 2010

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Inflammatory bowel diseases (IBD) increase the risk of developing colorectal cancer. Dietary components that reduce inflammation are associated with lower cancer risk. The long-chain omega-3 fatty acid docosahexaenoic acid (DHA) is present in fish oil and has potent anti-inflammatory properties. The objective of this study is to determine whether dietary fish oil enriched with DHA (DFO) could reduce experimentally induced colitis and colon cancer risk in a mouse model. When SMAD3−/− mice are exposed to Helicobacter hepaticus, mild colitis is observed 4 weeks postinfection. Mice were fed isocaloric diets modified to include corn oil, safflower oil, or DFO (doses ranging from 0.75% to 6.00%) as the fatty acid source for 8 weeks. Mice were gavaged with H. hepaticus; DFO feeding was continued; and mice were sacrificed 4 weeks after infection. The colon and cecum were collected for histopathology. Spleens and mesenteric lymph nodes were collected and analyzed for T-cell populations using flow cytometry. Contrary to expectations, DFO induced severe colitis and adenocarcinoma formation. DFO consumption was associated with decreased CD8 + cell frequency and diminished CD69 expression on CD4 + and CD8 + T-cell populations. Mice consuming DFO also exhibited higher FoxP3 + CD25 + CD4 + T regulatory cell frequency, FoxP3 expression, and altered L-selectin expression during infection. We concluded that DFO-fed mice may be less equipped to mount a successful response to H. hepaticus infection, increasing colon cancer risk. These results support the need to establish a tolerable upper limit for DHA intake particularly in the context of chronic inflammatory conditions such as IBD.

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Anti-inflammatory effects of enteral diet components on Crohn's disease-affected tissues in vitro

Cited by 62 publications

References 28 publications

The major pathway by which polymeric formula reduces inflammation in intestinal epithelial cells: a microarray-based analysis

The major pathway by which polymeric formula reduces inflammation in intestinal epithelial cells: a microarray-based analysis

Effect of exclusive enteral nutrition on bone turnover in children with Crohn’s disease

Dietary Fish Oil Alters T Lymphocyte Cell Populations and Exacerbates Disease in a Mouse Model of Inflammatory Colitis

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