Effects of vedolizumab, adalimumab and infliximab on biliary inflammation in individuals with primary sclerosing cholangitis and inflammatory bowel disease

2018 ◽  
Vol 48 (2) ◽  
pp. 190-195 ◽  
Author(s):  
C. S. Tse ◽  
E. V. Loftus ◽  
L. E. Raffals ◽  
A. A. Gossard ◽  
A. L. Lightner
2020 ◽  
Vol 158 (6) ◽  
pp. S-732-S-733
Author(s):  
Camilla A. Martins ◽  
Ana Elisa R. Caon ◽  
Marilia G. Cruz ◽  
Luísa L. Barros ◽  
Alexandre Carlos ◽  
...  

2018 ◽  
Vol 2 (8) ◽  
pp. 960-971 ◽  
Author(s):  
Brian K. Chung ◽  
Eva Kristine Klemsdal Henriksen ◽  
Kristin Kaasen Jørgensen ◽  
Tom H. Karlsen ◽  
Gideon M. Hirschfield ◽  
...  

2009 ◽  
Vol 136 (5) ◽  
pp. A-203
Author(s):  
Ashwin N. Ananthakrishnan ◽  
Dawn B. Beaulieu ◽  
Amar S. Naik ◽  
Yelena Zadvornova ◽  
Susan Skaros ◽  
...  

2020 ◽  
Vol 14 (7) ◽  
pp. 935-947 ◽  
Author(s):  
Mohammed Nabil Quraishi ◽  
Animesh Acharjee ◽  
Andrew D Beggs ◽  
Richard Horniblow ◽  
Chris Tselepis ◽  
...  

Abstract Background Although a majority of patients with PSC have colitis [PSC-IBD; primary sclerosing cholangitis-inflammatory bowel disease], this is phenotypically different from ulcerative colitis [UC]. We sought to define further the pathophysiological differences between PSC-IBD and UC, by applying a comparative and integrative approach to colonic gene expression, gut microbiota and immune infiltration data. Methods Colonic biopsies were collected from patients with PSC-IBD [n = 10], UC [n = 10], and healthy controls [HC; n = 10]. Shotgun RNA-sequencing for differentially expressed colonic mucosal genes [DEGs], 16S rRNA analysis for microbial profiling, and immunophenotyping were performed followed by multi-omic integration. Results The colonic transcriptome differed significantly between groups [p = 0.01]. Colonic transcriptomes from HC were different from both UC [1343 DEGs] and PSC-IBD [4312 DEGs]. Of these genes, only 939 had shared differential gene expression in both UC and PSC-IBD compared with HC. Imputed pathways were predominantly associated with upregulation of immune response and microbial defense in both disease cohorts compared with HC. There were 1692 DEGs between PSC-IBD and UC. Bile acid signalling pathways were upregulated in PSC-IBD compared with UC [p = 0.02]. Microbiota profiles were different between the three groups [p = 0.01]; with inferred function in PSC-IBD also being consistent with dysregulation of bile acid metabolism. Th17 cells and IL17-producing CD4 cells were increased in both PSC-IBD and UC when compared with HC [p < 0.05]. Multi-omic integration revealed networks involved in bile acid homeostasis and cancer regulation in PSC-IBD. Conclusions Colonic transcriptomic and microbiota analysis in PSC-IBD point toward dysregulation of colonic bile acid homeostasis compared with UC. This highlights important mechanisms and suggests the possibility of novel approaches in treating PSC-IBD.


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