In studies with mice, scientists have found evidence that osteoporosis-like bone disorders and inflammatory intestinal disorders are both caused by the abnormal regulation of a common protein.
Image by Brian Giesen via Flickr
Image by Brian Giesen via Flickr
Dr. Simon R. Carding from the University of Leeds in England and colleagues report their study in the December issue of the journal Immunity. Autoimmune-related bone disease and intestinal inflammation are closely linked with the deregulation and the hyperactivation CD4 T cells, which are involved in the body’s defense system, or immune response, they report. “How these T cells are activated and mediate disease is not clear.”
Mice that were genetically engineered to lack a key regulator of CD4 T cells have overactive T cells and spontaneously develop ulcerative colitis and the loss of bone cells, the scientists explain. Carding and colleagues’ experiments indicate that this is caused by increased production of a protein called RANKL.
“We find that the hyperactive CD4 T cells produce too much of this protein, which then contributes to bone breakdown and bowel inflammation,” Carding said.
Treating mice with osteoprotegerin, a protein that prevents RANKL from binding to its receptor, reversed this bone loss and improved colitis. “This study shows that some bone diseases and intestinal problems may share a common cause,” Carding told.
“If similar mechanisms occur in humans, then osteoprotegerin might prove a useful treatment for intestinal disorders such as ulcerative colitis and Crohn’s disease,” he said, which are both often accompanied by bone loss.
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