<i>Butyricicoccus pullicaecorum</i>in inflammatory bowel disease

Eeckhaut, Venessa; Machiels, Kathleen; Perrier, Clémentine; Romero, Claudia; Maes, S.; Flahou, Bram; Steppe, M; Haesebrouck, Freddy; Sas, Benedikt; Ducatelle, Richard; Vermeire, Séverine; Immerseel, Filip Van

doi:10.1136/gutjnl-2012-303611

Cited by 292 publications

(192 citation statements)

References 52 publications

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“…In addition, several recent studies focusing on the role of orally given butyrate producing bacteria like Butyricicoccus spp. or Clostridium tyrobutyricum, have revealed that the bacteria increase the butyrate levels in the colon and subsequently cure UC (Hudcovic et al, 2012;Eeckhaut et al, 2013). All these facts and our own results in this study consistently indicate that orally given butyrate could be a potential route to treat UC.…”

Section: Discussionsupporting

confidence: 74%

Intraperitoneal administration of butyrate prevents the severity of acetic acid colitis in rats

Malago

Sangu²

2015

J. Zhejiang Univ. Sci. B

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Intrarectal infusion of butyrate improves colorectal disorders including ulcerative colitis (UC). However, it is not established whether systemically administered butyrate benefits such patients. The current study aimed at exploring and comparing the potential of intraperitoneally, intrarectally, and orally administered butyrate against acetic acid (AA)-induced UC in rats. Intrarectal administration of 2 ml of 50% AA was done after or without prior treatment of rats for 7 consecutive days with 100 mg/kg sodium butyrate (SB) intraperitoneally, intrarectally, or orally. Rats were sacrificed after 48 h of AA-treatment. Subsequently, colon sections were processed routinely for histopathological examination. We clinically observed diarrhea, loose stools, and hemoccult-positive stools, and histologically, epithelial loss and ulceration, crypt damage, goblet cell depletion, hemorrhage, and mucosal infiltration of inflammatory cells. The changes were significantly reduced by intraperitoneal, intrarectal, or oral butyrate, with intraperitoneal butyrate exhibiting the highest potency. It is concluded that intraperitoneal administration of butyrate abrogates the lesions of AA-induced UC and its potency surpasses that of intrarectal or oral butyrate.

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Section: Discussionsupporting

confidence: 74%

Intraperitoneal administration of butyrate prevents the severity of acetic acid colitis in rats

Malago

Sangu²

2015

J. Zhejiang Univ. Sci. B

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“…Administration of butyrate-producing Clostridia such as F. prausnitzii and Butyricicoccus pullicaecorum to animal models of inflammation seems to lower the occurrence of macroscopic lesions to the intestinal mucosa 50,51 . Observations in model systems in vitro, animal models and healthy human individuals indicate that F. prausnitzii, in particular, resides preferentially close to the gut epithelium 52 .…”

Section: Regulation Of Intestinal Immunitymentioning

confidence: 99%

How the microbiota shapes rheumatic diseases

et al. 2016

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The human gut harbours a tremendously diverse and abundant microbial community that correlates with, and even modulates, many health-related processes. The mucosal interfaces are particularly active sites of microorganism-host interplay. Growing insight into the characteristic composition and functionality of the mucosal microbiota has revealed that the microbiota is involved in mucosal barrier integrity and immune function. This involvement affects proinflammatory and anti-inflammatory processes not only at the epithelial level, but also at remote sites such as the joints. Here, we review the role of the gut microbiota in shaping local and systemic immune responses and how disturbances in the host-microorganism interplay can potentially affect the development and progression of rheumatic diseases. Increasing our understanding of how to promote host-microorganism homeostasis could therefore reveal novel strategies for the prevention or alleviation of rheumatic disease.

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“…For example, recent studies investigating dysbiosis in patients with IBD identified lower levels of colonic butyrate and reduced abundance of butyrate-producing organisms (e.g., certain Faecalibacterium and Roseburia genera) with disease (84)(85)(86). The importance of butyrate as the preferred epithelial substrate has been highlighted by the finding that mice with mitochondrial polymorphisms resulting in increased oxidative phosphorylation activity are resistant to colitis (87) and inhibition of β-oxidation elicits colitis-like symptoms (88).…”

Section: Host-microbial Metabolism and Tissue Barriermentioning

confidence: 99%