{"id":1075,"date":"2024-08-16T13:54:15","date_gmt":"2024-08-16T13:54:15","guid":{"rendered":"https:\/\/www.microplanet.at\/?page_id=1075"},"modified":"2025-06-16T11:19:37","modified_gmt":"2025-06-16T10:19:37","slug":"preprints","status":"publish","type":"page","link":"https:\/\/www.microplanet.at\/index.php\/preprints\/","title":{"rendered":"Preprints"},"content":{"rendered":"\n
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Preprints<\/h2><\/div>\n<\/section>\n\n\n\n
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Preprints of key researchers of our CoE – since 2024<\/h2>\n\n\n
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Baumgartner, Maximilian; Schnaufer, Franziska; Duquesnoy, Maeva; Asatsuma, Takahiro; Chakrabarty, Adrija; Frick, Adrian; Fuchs, Claudia; Gerstorfer, Michael; Hains, Patrik; K\u00f6cher, Thomas; Schimmel, Patrick; Lichtenstein, Mauriz A.; Leistl, Sofia; Pinter, Felix; Krstevska, Elena; Nyein, Thet Khaing; H\u00f6genauer, Christoph; Makristathis, Athanasios; Gasche, Christoph; Primas, Christian; Reinisch, Walter; Winter, Georg E.; Trauner, Michael; G\u00fcnther, Claudia; Busslinger, Georg; Gorkiewicz, Gregor; Chassaing, Benoit; Campbell, Clarissa<\/p>

Host-derived bile acids drive dysbiosis by selecting bile-resistant epimerizing bacteria in inflammatory bowel disease<\/a> Unpublished<\/span> <\/p>

bioRxiv, <\/span>2026<\/span>.<\/p>

Abstract<\/a><\/span> | Links<\/a><\/span> | BibTeX<\/a><\/span><\/p>

@unpublished{Baumgartner2026,
\r\ntitle = {Host-derived bile acids drive dysbiosis by selecting bile-resistant epimerizing bacteria in inflammatory bowel disease},
\r\nauthor = {Maximilian Baumgartner and Franziska Schnaufer and Maeva Duquesnoy and Takahiro Asatsuma and Adrija Chakrabarty and Adrian Frick and Claudia Fuchs and Michael Gerstorfer and Patrik Hains and Thomas K\u00f6cher and Patrick Schimmel and Mauriz A. Lichtenstein and Sofia Leistl and Felix Pinter and Elena Krstevska and Thet Khaing Nyein and Christoph H\u00f6genauer and Athanasios Makristathis and Christoph Gasche and Christian Primas and Walter Reinisch and Georg E. Winter and Michael Trauner and Claudia G\u00fcnther and Georg Busslinger and Gregor Gorkiewicz and Benoit Chassaing and Clarissa Campbell},
\r\nurl = {http:\/\/biorxiv.org\/lookup\/doi\/10.64898\/2026.06.18.733240},
\r\ndoi = {10.64898\/2026.06.18.733240},
\r\nyear  = {2026},
\r\ndate = {2026-06-19},
\r\nurldate = {2026-06-19},
\r\npublisher = {openRxiv},
\r\nabstract = {<jats:title>Abstract<\/jats:title>
\r\n                <jats:p>Microbial dysbiosis is a hallmark of inflammatory bowel diseases (IBD); however, its drivers and impact on disease pathophysiology are poorly understood. Applying neural network-based feature attribution to metabolomics and metagenomics datasets from >5000 individuals, we identified epimerized host derived bile acids (BAs) produced by microbial hydroxysteroid dehydrogenases (HSDHs) as a novel hallmark of IBD-associated dysbiosis. Epimerized BAs reduce FXR activity in intestinal epithelial cells and dampen their production of FGF19, a negative feedback regulator of host-derived bile acid (HBA) production in the liver. Increased HBA levels drive colonic epithelial remodeling by impacting goblet cell maturation and select for HSDH-carrying bacteria that transform bactericidal HBA into less toxic, epimerized forms. Confirming the translational relevance of these findings, we demonstrated that high HBA levels limit fecal microbiota transplant engraftment and show that BA sequestering drugs support microbiome recovery in patients with high HBA levels. Together, we discover that elevated HBAs deplete BA-sensitive commensals and favor the growth of HSDH-encoding pathobionts that disrupt host BA feedback signaling, establishing a causal link between changes in microbial ecology and IBD pathophysiology.<\/jats:p>},
\r\nhowpublished = {bioRxiv},
\r\nkeywords = {},
\r\npubstate = {published},
\r\ntppubtype = {unpublished}
\r\n}
\r\n<\/pre><\/div>
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<jats:title>Abstract<\/jats:title>
\r\n                <jats:p>Microbial dysbiosis is a hallmark of inflammatory bowel diseases (IBD); however, its drivers and impact on disease pathophysiology are poorly understood. Applying neural network-based feature attribution to metabolomics and metagenomics datasets from >5000 individuals, we identified epimerized host derived bile acids (BAs) produced by microbial hydroxysteroid dehydrogenases (HSDHs) as a novel hallmark of IBD-associated dysbiosis. Epimerized BAs reduce FXR activity in intestinal epithelial cells and dampen their production of FGF19, a negative feedback regulator of host-derived bile acid (HBA) production in the liver. Increased HBA levels drive colonic epithelial remodeling by impacting goblet cell maturation and select for HSDH-carrying bacteria that transform bactericidal HBA into less toxic, epimerized forms. Confirming the translational relevance of these findings, we demonstrated that high HBA levels limit fecal microbiota transplant engraftment and show that BA sequestering drugs support microbiome recovery in patients with high HBA levels. Together, we discover that elevated HBAs deplete BA-sensitive commensals and favor the growth of HSDH-encoding pathobionts that disrupt host BA feedback signaling, establishing a causal link between changes in microbial ecology and IBD pathophysiology.<\/jats:p><\/div>
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