Investigating micronutrients and epigenetic mechanisms in relation to inflammatory bowel disease

Barnett, Matthew P. G.; Bermingham, Emma N.; McNabb, Warren C.; Bassett, Shalome A.; Armstrong, Kelly; Rounce, J. R.; Roy, Nicole C.

doi:10.1016/j.mrfmmm.2010.02.006

Cited by 36 publications

(34 citation statements)

References 134 publications

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“…In addition, a recent study in rats demonstrated that increasing dietary Se using basal diets (Se-deficient) supplemented with l-Se-Met at 0.15 ppm (Se-adequate) or 4 ppm (above-adequate) for 104 days decreased global genomic DNA methylation in liver and colon mucosa, with specific genes particularly sensitive to this effect (280). In fact, Se and other dietary factors have been shown to affect epigenetic mechanisms related to cancer (13). There are findings indicating that dietary Se influence epigenetic mechanisms involved in cancer and that nutrient interactions are important in cancer susceptibility (50).…”

Section: Epigenetic Poising In Naive T Helper Cells Does Se Intake Amentioning

confidence: 99%

“…Chronic inflammation may be an underlying risk factor in the early stages of cancer development, as well as being a key feature of inflammatory bowel disease (IBD). In fact, levels and interactions between nutrients have been shown to impact the epigentic regulation of IBD (13). Overall, Se status may influence the poising of naive CD4 + T cells through redox intermediates that epigenetically influence differentiation toward a particular phenotype upon TCR-engagement (Fig.…”

Section: Fig 11 Analyses Of Cell Markers During Activation Of Naivementioning

confidence: 99%

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The Role of Selenium in Inflammation and Immunity: From Molecular Mechanisms to Therapeutic Opportunities

Huang

Rose

Hoffmann

2012

Antioxidants & Redox Signaling

710

496

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Dietary selenium (]Se), mainly through its incorporation into selenoproteins, plays an important role in inflammation and immunity. Adequate levels of Se are important for initiating immunity, but they are also involved in regulating excessive immune responses and chronic inflammation. Evidence has emerged regarding roles for individual selenoproteins in regulating inflammation and immunity, and this has provided important insight into mechanisms by which Se influences these processes. Se deficiency has long been recognized to negatively impact immune cells during activation, differentiation, and proliferation. This is related to increased oxidative stress, but additional functions such as protein folding and calcium flux may also be impaired in immune cells under Se deficient conditions. Supplementing diets with above-adequate levels of Se can also impinge on immune cell function, with some types of inflammation and immunity particularly affected and sexually dimorphic effects of Se levels in some cases. In this comprehensivearticle, the roles of Se and individual selenoproteins in regulating immune cell signaling and function are discussed. Particular emphasis is given to how Se and selenoproteins are linked to redox signaling, oxidative burst, calcium flux, and the subsequent effector functions of immune cells. Data obtained from cell culture and animal models are reviewed and compared with those involving human physiology and pathophysiology, including the effects of Se levels on inflammatory or immune-related diseases including anti-viral immunity, autoimmunity, sepsis, allergic asthma, and chronic inflammatory disorders. Finally, the benefits and potential adverse effects of intervention with Se supplementation for various inflammatory or immune disorders are discussed. Antioxid. Redox Signal. 16, 705-743.

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Section: Epigenetic Poising In Naive T Helper Cells Does Se Intake Amentioning

confidence: 99%

Section: Fig 11 Analyses Of Cell Markers During Activation Of Naivementioning

confidence: 99%

The Role of Selenium in Inflammation and Immunity: From Molecular Mechanisms to Therapeutic Opportunities

Huang

Rose

Hoffmann

2012

Antioxidants & Redox Signaling

710

496

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“…Recent accumulation of data suggests that certain components in the diet have critical roles in the physiological development of the gut immune system (2,(5)(6)(7). Malnutrition is known to result in a higher susceptibility to intestinal infections or autoimmune-mediated gut inflammation (2,(8)(9)(10).…”

mentioning

confidence: 99%

Dietary Folic Acid Promotes Survival of Foxp3+ Regulatory T Cells in the Colon

Kinoshita

Kayama

Kusu

et al. 2012

The Journal of Immunology

118

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Dietary compounds as well as commensal microbiota contribute to the generation of a unique gut environment. In this study, we report that dietary folic acid (FA) is required for the maintenance of Foxp3+ regulatory T cells (Tregs) in the colon. Deficiency of FA in the diet resulted in marked reduction of Foxp3+ Tregs selectively in the colon. Blockade of folate receptor 4 and treatment with methotrexate, which inhibits folate metabolic pathways, decreased colonic Foxp3+ Tregs. Compared with splenic Tregs, colonic Tregs were more activated to proliferate vigorously and were highly sensitive to apoptosis. In colonic Tregs derived from mice fed with a FA-deficient diet, expression of anti-apoptotic molecules Bcl-2 and Bcl-xL was severely decreased. A general reduction of peripheral Tregs was induced by a neutralizing Ab against IL-2, but a further decrease by additional FA deficiency was observed exclusively in the colon. Mice fed with an FA-deficient diet exhibited higher susceptibility to intestinal inflammation. These findings reveal the previously unappreciated role of dietary FA in promotion of survival of Foxp3+ Tregs that are in a highly activated state in the colon.

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“…Among others a role for epigenetic changes has been suggested in the pathogenesis of Type 2 diabetes, chronic obstructive lung disease, chronic inflammatory bowel disease and atherosclerosis [55][56][57][58]. Complex gene-environment interactions might alter immune function and inflammatory response via changes in the epigenome and thereby promote the development of chronic diseases.…”

Section: Conclusion and Summarymentioning

confidence: 99%

Inflammatory memories: Is epigenetics the missing link to persistent stromal cell activation in rheumatoid arthritis?

Ospelt

Reedquist

Gay

et al. 2011

Autoimmunity Reviews

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Investigating micronutrients and epigenetic mechanisms in relation to inflammatory bowel disease

Cited by 36 publications

References 134 publications

The Role of Selenium in Inflammation and Immunity: From Molecular Mechanisms to Therapeutic Opportunities

The Role of Selenium in Inflammation and Immunity: From Molecular Mechanisms to Therapeutic Opportunities

Dietary Folic Acid Promotes Survival of Foxp3+ Regulatory T Cells in the Colon

Inflammatory memories: Is epigenetics the missing link to persistent stromal cell activation in rheumatoid arthritis?

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