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1.
Nat Med ; 25(4): 701, 2019 Apr.
Article in English | MEDLINE | ID: mdl-30846883

ABSTRACT

Owing to an error during typesetting, a number of references were deleted from the Methods reference list. This altered all of the references in the Methods section and some of the references in Extended Data Fig. 5, making them inaccurate. References 121-134 were added back into the Methods reference list, and the references in the Methods section and in Extended Data Fig. 5 were renumbered accordingly. The error has been corrected in the PDF and HTML versions of this article.

2.
Nat Med ; 25(2): 323-336, 2019 02.
Article in English | MEDLINE | ID: mdl-30664783

ABSTRACT

Inflammatory bowel diseases (IBD) can be broadly divided into Crohn's disease (CD) and ulcerative colitis (UC) from their clinical phenotypes. Over 150 host susceptibility genes have been described, although most overlap between CD, UC and their subtypes, and they do not adequately account for the overall incidence or the highly variable severity of disease. Replicating key findings between two long-term IBD cohorts, we have defined distinct networks of taxa associations within intestinal biopsies of CD and UC patients. Disturbances in an association network containing taxa of the Lachnospiraceae and Ruminococcaceae families, typically producing short chain fatty acids, characterize frequently relapsing disease and poor responses to treatment with anti-TNF-α therapeutic antibodies. Alterations of taxa within this network also characterize risk of later disease recurrence of patients in remission after the active inflamed segment of CD has been surgically removed.


Subject(s)
Crohn Disease/microbiology , Gastrointestinal Microbiome , Adrenal Cortex Hormones/therapeutic use , Case-Control Studies , Colitis, Ulcerative/diagnosis , Colitis, Ulcerative/drug therapy , Colitis, Ulcerative/microbiology , Colitis, Ulcerative/surgery , Crohn Disease/diagnosis , Crohn Disease/drug therapy , Crohn Disease/surgery , Humans , Recurrence , Tumor Necrosis Factor-alpha/antagonists & inhibitors , Tumor Necrosis Factor-alpha/metabolism
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