Crohn’s disease and ulcerative colitis are the most common forms of inflammatory bowel disease (IBD). Although IBD is thought to be caused by an inappropriate immune response to the bacteria living naturally in the gut, exactly how bacteria trigger this response is not known.
Now, in a study appearing online on October 5 in advance of publication in the November print issue of the Journal of Clinical Investigation, researchers from the University of Philadelphia have shown that mice lacking the protein RELM-beta are protected from colitis induced by ingestion of dextran sodium sulfate (DSS).
Previous studies have shown that bacteria in the gut induce cells of the intestine to produce RELM-beta. So, David Wu and colleagues set out to investigate whether this protein had a role in IBD. They found that mice lacking RELM-beta were protected from DSS-induced colitis and that RELM-beta was highly expressed in the colon of mice that spontaneously develop an IBD-like disease.
As RELM-beta was found to activate macrophages to produce pro-inflammatory factors both in vitro and in vivo, the authors suggest that RELM-beta is one important link between bacteria and the onset of IBD.
