Dysbiosis modulates capacity for bile acid modification in the gut microbiomes of patients with inflammatory bowel disease: a mechanism and marker of disease? - PubMed (original) (raw)

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Dysbiosis modulates capacity for bile acid modification in the gut microbiomes of patients with inflammatory bowel disease: a mechanism and marker of disease?

Lesley A Ogilvie et al. Gut. 2012 Nov.

Free PMC article

No abstract available

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Conflict of interest statement

Competing interests: None.

Figures

Figure 1

Bile salt hydrolase (BSH) relative abundance profiles for major phylogenetic divisions in the human gut microbiota. ACT, Actinobacteria; BACT, Bacteroidetes; FIRM, Firmicutes; TOTAL, BSH-like relative abundance in complete MetaHIT dataset regardless of phylogenetic affiliation. ALL MH, complete MetaHIT dataset, HEALTHY, healthy individuals only, UC, individuals with ulcerative colitis only, CD, individuals with Crohn's disease only. Error bars indicate SEM. Level of significance in χ2 distribution analysis: *p<0.01, **p<0.001. Inset table shows relative abundance, within complete MH dataset, for other phylogenetic divisions with which BSH-like homologues were affiliated. Brackets denote SEM.

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Farnesoid X receptor activation inhibits inflammation and preserves the intestinal barrier in inflammatory bowel disease.
Gadaleta RM, van Erpecum KJ, Oldenburg B, Willemsen EC, Renooij W, Murzilli S, Klomp LW, Siersema PD, Schipper ME, Danese S, Penna G, Laverny G, Adorini L, Moschetta A, van Mil SW. Gadaleta RM, et al. Gut. 2011 Apr;60(4):463-72. doi: 10.1136/gut.2010.212159. Epub 2011 Jan 17. Gut. 2011. PMID: 21242261

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Dysbiosis modulates capacity for bile acid modification in the gut microbiomes of patients with inflammatory bowel disease: a mechanism and marker of disease? - PubMed (original) (raw)