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Microbiota as a cornerstone in the development of primary sclerosing cholangitis: paving the path for translational diagnostic and therapeutic approaches
  1. Catherine Mooser,
  2. Stephanie Christine Ganal-Vonarburg
  1. Department for BioMedical Research, University of Bern, Bern, Switzerland
  1. Correspondence to Dr Catherine Mooser, Department for BioMedical Research (DBMR), University of Bern, 3008 Bern, Switzerland ; catherine.mooser{at}

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In the last decades, the proportion of host–microbiota interaction studies in biomedical research continuously increased, mainly driven by the quest for a better understanding of microbiota-associated human diseases. Among the numerous medical conditions the courses of which have been shown to be influenced by the microbiota, GI disorders and especially IBDs have been studied extensively, either in experimental murine models or in clinical studies (reviewed in ref 1). Among the plethora of immune pathways impacted and dysregulated by the microbiota and thus leading to pathologies, inflammasome signalling has been shown to severely affect the progression of GI disorders2 and to be associated with microbiota composition.3 Primary sclerosing cholangitis (PSC) represents a rare disease characterised by chronic inflammation and concomitant fibrosis of the biliary tree with a poor outcome. A microbiota-dependent pathogenesis of PSC, similar to that of IBD, has been suggested.4 However, the number of clinical and experimental studies addressing host–microbiota interactions in PSC remains limited. Rederivation of PSC models into germ-free conditions caused either attenuation or aggravation of the phenotype,5 emphasising the microbiota-dependent character of this pathology and …

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  • Contributors CM and SCGV wrote the manuscript.

  • Funding CM received an MD-PhD fellowship of the Swiss National Science Foundation (323530_158124). SCGV is supported by the Directorate for Teaching and Research of the Inselspital and by the Johanna Dürmüller-Bol Foundation.

  • Competing interests None declared.

  • Provenance and peer review Commissioned; internally peer reviewed.

  • Patient consent for publication Not required.

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