Biotin effects in Chrohn's disease

Okabe, Nobuhiko; Urabe, Katsuhiko; Fujita, Köichi; Yamamoto, Tetsuya; Yao, Tsuneyoshi; Doi, Shingo

doi:10.1007/bf01537009

Cited by 23 publications

(14 citation statements)

References 5 publications

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“…These cells play an important role in promoting antipathogen responses and in maintaining intestinal epithelial homeostasis (43). It is worth mentioning here that activity of these cells and level of biotin are both decreased in patients with Crohn's disease (2,13,23,24,43). Further studies are needed to delineate the mechanism(s) involved in the inflammatory responses observed in the intestine of the SMVT KO mice.…”

Section: Discussionmentioning

confidence: 92%

“…In the cecum of the KO mice, chronic active inflammation with focal cryptitis/crypt abscesses, as well as low-grade adenomatous changes and extensive submucosal edema, were observed although the mechanisms that mediate these inflammatory responses in the SMVT KO mice are under ). An example of the latter is the essentiality of biotin for normal activity of intestinal NK cells (24). These cells play an important role in promoting antipathogen responses and in maintaining intestinal epithelial homeostasis (43).…”

Section: Discussionmentioning

confidence: 99%

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Conditional knockout of the Slc5a6 gene in mouse intestine impairs biotin absorption

Ghosal¹,

Lambrecht²,

Subramanya³

et al. 2013

American Journal of Physiology-Gastrointestinal and Liver Physi

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gene expresses a plasma membrane protein involved in the transport of the watersoluble vitamin biotin; the transporter is commonly referred to as the sodium-dependent multivitamin transporter (SMVT) because it also transports pantothenic acid and lipoic acid. The relative contribution of the SMVT system toward carrier-mediated biotin uptake in the native intestine in vivo has not been established. We used a Cre/lox technology to generate an intestine-specific (conditional) SMVT knockout (KO) mouse model to address this issue. The KO mice exhibited absence of expression of SMVT in the intestine compared with sex-matched littermates as well as the expected normal SMVT expression in other tissues. About two-thirds of the KO mice died prematurely between the age of 6 and 10 wk. Growth retardation, decreased bone density, decreased bone length, and decreased biotin status were observed in the KO mice. Microscopic analysis showed histological abnormalities in the small bowel (shortened villi, dysplasia) and cecum (chronic active inflammation, dysplasia) of the KO mice. In vivo (and in vitro) transport studies showed complete inhibition in carrier-mediated biotin uptake in the intestine of the KO mice compared with their control littermates. These studies provide the first in vivo confirmation in native intestine that SMVT is solely responsible for intestinal biotin uptake. These studies also provide evidence for a casual association between SMVT function and normal intestinal health.

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Section: Discussionmentioning

confidence: 92%

Section: Discussionmentioning

confidence: 99%

Conditional knockout of the Slc5a6 gene in mouse intestine impairs biotin absorption

Ghosal¹,

Lambrecht²,

Subramanya³

et al. 2013

American Journal of Physiology-Gastrointestinal and Liver Physi

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show abstract

“…Furthermore, biotin deficiency is observed in patients with Crohn’s disease (32). Th1 and Th17 cells are well established as significant players in Crohn’s disease and colitis (33, 34).…”

Section: Discussionmentioning

confidence: 99%

Biotin Deficiency Induces Th1- and Th17-Mediated Proinflammatory Responses in Human CD4+ T Lymphocytes via Activation of the mTOR Signaling Pathway

Elahi

Sabui

Narasappa

et al. 2018

The Journal of Immunology

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Biotin (vitamin B7) is essential for human health because of its involvement, as a cofactor, in a variety of critical cellular metabolic reactions. Previous studies have shown that biotin deficiency enhances inflammation, and certain chronic inflammatory diseases are associated with biotin deficiency; however, the mechanisms that mediate the association between biotin status and inflammation are not well understood. In this study, we examined the effect of biotin deficiency on human CD4+ T cell responses to determine their role in biotin deficiency–associated inflammation. Our investigations revealed that anti-CD3/CD28–stimulated CD4+ T cells cultured in biotin-deficient medium secreted significantly enhanced levels of the proinflammatory cytokines IFN-γ, TNF, and IL-17. Expression of the transcription factors T-bet and RORγt was increased, whereas Foxp3 expression was decreased, in biotin-deficient CD4+ T cells. The percentage of T regulatory cells was also decreased under biotin-deficient condition. A similar increase in T-bet, RORγt, and proinflammatory cytokine levels, as well as a decrease in Foxp3, was observed in inguinal lymph nodes of mice fed a biotin-deficient diet relative to pair-fed controls. Furthermore, differentiation of CD4+ T cells toward Th1 and Th17 cells was also enhanced. In vitro and in vivo investigations indicated that the increased inflammatory response was due to enhanced activation of the mammalian target of rapamycin signaling pathway in biotin-deficient CD4+ T cells. In summary, these results demonstrate that biotin deficiency enhances the inflammatory responses in CD4+ T cells, which may contribute to inflammation associated with biotin deficiency.

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“…For example, 90% of patients with pellagra, who have vitamin B 6 deficiency, suffer from colitis . Biotin regulates activity of natural killer cells, which is reduced, along with systemic biotin levels, in patients with Crohn's disease . This association between inflammatory gut diseases and vitamin deficiencies may be explained by the importance of these vitamins and other micronutrients for colonocyte function with respect to the mucosal barrier and the local immune system.…”

Section: Impact On the Innate Immune Systemmentioning

confidence: 99%

Nutrition meets the microbiome: micronutrients and the microbiota

Biesalski

2016

Annals of the New York Academy of Sciences

195

131

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There is increasing evidence that food is an important factor that influences and shapes the composition and configuration of the gut microbiota. Most studies have focused on macronutrients (fat, carbohydrate, protein) in particular and their effects on the gut microbiota. Although the microbiota can synthesize different water-soluble vitamins, the effects of vitamins synthesized within the microbiota on systemic vitamin status are unclear. Few studies exist on the shuttling of vitamins between the microbiota and intestine and the impact of luminal vitamins on the microbiota. Studying the interactions between vitamins and the microbiota may help to understand the effects of vitamins on the barrier function and immune system of the intestinal tract. Furthermore, understanding the impact of malnutrition, particularly low micronutrient supply, on microbiota development, composition, and metabolism may help in implementing new strategies to overcome the deleterious effects of malnutrition on child development. This article reviews data on the synthesis of different micronutrients and their effects on the human microbiota, and further discusses the consequences of malnutrition on microbiota composition.

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Biotin effects in Chrohn's disease

Cited by 23 publications

References 5 publications

Conditional knockout of the Slc5a6 gene in mouse intestine impairs biotin absorption

Conditional knockout of the Slc5a6 gene in mouse intestine impairs biotin absorption

Biotin Deficiency Induces Th1- and Th17-Mediated Proinflammatory Responses in Human CD4+ T Lymphocytes via Activation of the mTOR Signaling Pathway

Nutrition meets the microbiome: micronutrients and the microbiota

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