Tumor Necrosis Factor α Reduces Butyrate Oxidation In Vitro in Human Colonic Mucosa: A Link from Inflammatory Process to Mucosal Damage?

Nancey, Stéphane; Moussata, Driffa; Graber, I. G.; Claudel, Sylvette; Saurin, Jean‐Christophe; Flourié, Bernard

doi:10.1097/01.mib.0000161918.04760.f3

Cited by 22 publications

(15 citation statements)

References 70 publications

(137 reference statements)

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“…Studies of GPR43 −/− mice demonstrate a role for this G-protein-coupled receptor in regulating inflammatory responses in a murine model of colitis, suggesting that host sensing of SCFA is important for host-microbial homeostasis (29). Furthermore, proinflammatory cytokines, such as TNF-α, can impair butyrate oxidation by the colonic mucosa, and increasing luminal levels may be beneficial (30).…”

Section: Discussionmentioning

confidence: 99%

Bifidobacterium animalis subsp. lactis fermented milk product reduces inflammation by altering a niche for colitogenic microbes

Veiga

Gallini

Beal

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

202

164

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Intestinal health requires the coexistence of eukaryotic self with the gut microbiota and dysregulated host-microbial interactions can result in intestinal inflammation. Here, we show that colitis improved in T-bet −/− Rag2 −/− mice that consumed a fermented milk product containing Bifidobacterium animalis subsp. lactis DN-173 010 strain. A decrease in cecal pH and alterations in short chain fatty acid profiles occurred with consumption, and there were concomitant increases in the abundance of select lactate-consuming and butyrate-producing bacteria. These metabolic shifts created a nonpermissive environment for the Enterobacteriaceae recently identified as colitogenic in a T-bet −/− Rag2 −/− ulcerative colitis mouse model. In addition, 16S rRNA-based analysis of the T-bet −/− Rag2 −/− fecal microbiota suggest that the structure of the endogenous gut microbiota played a key role in shaping the host response to the bacterial strains studied herein. We have identified features of the gut microbiota, at the membership and functional level, associated with response to this B. lactis -containing fermented milk product, and therefore this model provides a framework for evaluating and optimizing probiotic-based functional foods.

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Section: Discussionmentioning

confidence: 99%

Bifidobacterium animalis subsp. lactis fermented milk product reduces inflammation by altering a niche for colitogenic microbes

Veiga

Gallini

Beal

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

202

164

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“…A possible explanation for the decreased oxidation in UC patients was proposed by Nancey et al who showed that butyrate oxidation could be reduced by TNFa at concentrations found in inflamed human mucosa. 104 It has also been reported that butyrate oxidation in colonocytes can be inhibited by hydrogen sulphide in vitro. 105 Increased luminal concentrations of sulphide as well as high numbers of sulphate-reducing bacteria have been reported in UC patients.…”

Section: Butyrate and Inflammationmentioning

confidence: 96%

Review article: the role of butyrate on colonic function

Hamer¹,

Jonkers²,

Venema³

et al. 2007

Aliment Pharmacol Ther

2,266

1,612

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“…However, others report absence of cytotoxicity upon addition of pro‐inflammatory cytokines to epithelial cells and colonic carcinoma cell lines (Nancey et al, ). For example, Nancey et al () found no changes in cell viability after a 2 h incubation with TNF‐α (range 100–5000 pg/ml) in human colonic biopsies or human colonocytes. Our data indicate that an inflammatory stimulation for 1 h with TNF‐α and/or IFN‐γ did not affect HT‐29 cell viability.…”

Section: Discussionmentioning

confidence: 99%

Inflammation‐Induced Downregulation of Butyrate Uptake and Oxidation Is Not Caused by a Reduced Gene Expression

Boesmans

Ramakers

Arijs

et al. 2014

Journal Cellular Physiology

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In ulcerative colitis (UC) the butyrate metabolism is impaired, leading to energy-deficiency in the colonic cells. The effect of inflammation on the butyrate metabolism was investigated. HT-29 cells were incubated with pro-inflammatory cytokines (TNF-α and/or IFN-γ) for 1 and 24 h. Cells were additionally stimulated with butyrate to investigate its anti-inflammatory potential. Butyrate uptake and oxidation were measured using (14)C-labeled butyrate. Gene expression of the butyrate metabolism enzymes, interleukin 8 (IL-8; inflammatory marker) and villin-1 (VIL-1; epithelial cell damage marker) was measured via quantitative RT-PCR. Significantly increased IL-8 expression and decreased VIL-1 expression after 24 h incubation with TNF-α and/or IFN-γ confirmed the presence of inflammation. These conditions induced a decrease of both butyrate uptake and oxidation, whereas the gene expression was not reduced. Simultaneous incubation with butyrate counteracted the reduced butyrate oxidation. In contrast, 1 h incubation with TNF-α induced a significant increased IL-8 expression and decreased butyrate uptake. Incubation with TNF-α and/or IFN-γ for 1 h did not induce cell damage nor influence butyrate oxidation. The inflammation-induced downregulation of the butyrate metabolism was not caused by a reduced gene expression, but appeared consequential to a decreased butyrate uptake. Increasing the luminal butyrate levels might have therapeutic potential in UC.

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Tumor Necrosis Factor α Reduces Butyrate Oxidation In Vitro in Human Colonic Mucosa: A Link from Inflammatory Process to Mucosal Damage?

Cited by 22 publications

References 70 publications

Bifidobacterium animalis subsp. lactis fermented milk product reduces inflammation by altering a niche for colitogenic microbes

Bifidobacterium animalis subsp. lactis fermented milk product reduces inflammation by altering a niche for colitogenic microbes

Review article: the role of butyrate on colonic function

Inflammation‐Induced Downregulation of Butyrate Uptake and Oxidation Is Not Caused by a Reduced Gene Expression

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