Profiling_the_role_of_the_gut_microbiota_in_IBD_2017-sc-4807
Profiling_the_role_of_the_gut_microbiota_in_IBD_2017
The human gut microbiota have been shown to be markedly different between healthy individuals and those with inflammatory bowel disease (IBD). It is less clear whether these differences reflect causal predisposition, or consequence of inflammation, or whether the microbiota might be responsible for relapses after a period of quiescent disease (so-called "flares"), or differential response to treatment.                                                                   The Genetics, Enviroment, Microbiome (GEM) study, which collects Crohn's patients with active disease, and firstdegree relatives as household controls. The goal of this study is to retrospectively analyse samples from the relatives in the subset that go on to develop Crohn's (a very rare event, even given a relative risk of ~20). We will instead take all ~300 paired cases and controls from the UK subset of this study and generate stool metagenomes.  This data is part of a pre-publication release. For information on the proper use of pre-publication data shared by the Wellcome Trust Sanger Institute please see http://www.sanger.ac.uk/datasharing/
The human gut microbiota have been shown to be markedly different between healthy individuals and those with inflammatory bowel disease (IBD). It is less clear whether these differences reflect causal predisposition, or consequence of inflammation, or whether the microbiota might be responsible for relapses after a period of quiescent disease (so-called "flares"), or differential response to treatment.                                                                   The Genetics, Enviroment, Microbiome (GEM) study, which collects Crohn's patients with active disease, and firstdegree relatives as household controls. The goal of this study is to retrospectively analyse samples from the relatives in the subset that go on to develop Crohn's (a very rare event, even given a relative risk of ~20). We will instead take all ~300 paired cases and controls from the UK subset of this study and generate stool metagenomes which will allow us to begin building matched case and control data