9+44 days. All patients required prolonged mechanical ventilation (mean duration: 45+28 days), with the need of extracorporal membrane oxygenation (ECMO) in 11 patients. Laboratory findings at the time Selleck Barasertib of ERCP were: bilirubin: 14.9[0.4-18]; (mg/dl, median[range]), GGT: 29[1.3-60.8] (xULN, median[range]), AP: 10.8[1.1-28.0], (xULN, median[range]). Sphincterotomy, extraction of casts/ sludge and dilations of dominant strictures were performed during ERCP. During follow up 26 patients died and 4 patients were transplanted. Number of organ failure and organ replacement therapy were independent risk factors for mortality. Conclusion: Critical reduction of hepatic oxygen delivery may lead to initial

bile duct injury in ICU patients. Vasopressor treatment and sedoanalgesia, hepatic ischemia, as well as translocation of endotoxins and bacteria from the gut may further perpetuate progressing SC-CIP, which

carries a high mortality as a high proportion of these patients rapidly develop liver cirrhosis and liver failure. Disclosures: Harald Hofer – Speaking and Teaching: Janssen, Roche, MSD, Gilead, Abbvie Peter Fickert – Consulting: Falk Foundation, Falk Foundation, Trichostatin A ic50 Falk Foundation, Falk Foundation; Speaking and Teaching: Roche Austria, Gilead Austria, MSD Austria, MERCK Austria, Roche Austria, Gilead Austria, MSD Austria, MERCK Austria, Roche Austria, Gilead Austria, MSD Austria, MERCK Austria, Roche Austria, Gilead Austria, MSD Austria, MERCK Austria Michael Trauner – Advisory Committees or Review Panels: MSD, Janssen, Gilead, Abbvie; Consulting: Phenex; Grant/Research Support: Intercept, Falk Pharma, Albireo; Patent Held/Filed: Med Uni Graz (norUDCA); Speaking and Teaching: Falk Foundation, Roche, Interleukin-3 receptor Gilead The following people have nothing to disclose: Gernot Zollner, Ivo Graziadei Background: dnTGFβRII mice develop high titer AMAs and histologic features characteristic of autoimmune cholangitis, with striking similarities to human PBC. There is increasing interest in the potential use of regulatory T cells (Tregs) as immunotherapy to treat

diseases characterized by loss of tolerance. We have taken advantage of the dnTGFβRII model and, in particular, an ability to induce autoimmune cholangitis in Rag1−/− recipients by adoptive transfer of dysregulated CD8+ T cells from dnT-GFβRII mice. Such adoptively transferred Rag1−/− recipients develop severe portal inflammation with both histologic and cytokine evidence of intense inflammation. Methods: Rag1−/− mice, at four weeks of age, received either CD8+ T cells from dnTGFβRII mice with co-transfer of either Foxp3+ Tregs derived from wild-type and otherwise healthy C57BL/6 mice, or dnTGFβRII mice. Recipient mice were monitored for histology including portal inflammation and intra-lobular biliary cell damage, phenotypic changes in recipient lymphoid populations and local and systemic cytokine production.