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Bone Marrow Holds Secrets for Treating Colitis and Crohn's

Michigan State University researchers have unlocked secrets in bone marrow that could lead to improved treatments for colitis and Crohn's disease.


The results, featured in the current issue of Proceedings of the National Academy of the Sciences, show that the havoc inflammatory bowel diseases wreaks on the digestive tract is mirrored in bone marrow. Early indications also show that the disorders of the gut could potentially be treated through the bone marrow, said Pam Fraker, MSU University Distinguished Professor of biochemistry and molecular biology.

"It's possible that if we could reduce bone marrow's ability to produce inflammatory cells that we could reduce the severity of colitis and Crohn's disease," said Fraker, who co-authored the study with MSU colleagues Laura McCabe, professor of physiology and radiology, and Mark Trottier, research specialist. "This could limit the damage that the disease causes and reduce the number of patients needing surgery."

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First Evidence for a Genetic Cause for Barrett's Esophagus

Genetic variations that are linked with the onset of Barrett's esophagus (BE), a pre-cancerous condition of the lower end of the gullet, have been identified for the first time. The discovery of variations in regions on two chromosomes makes it possible to develop screening tests for people at high risk of developing the disease.

Although it's been thought for some time that there may be genetic causes for BE as well as environmental ones, such as drinking alcohol and eating fatty food, so far researchers have not found any genetic variations that are associated with the condition.

Now, a multi-national team of researchers led by Professor Janusz Jankowski of the Blizard Institute of Cell and Molecular Science at Queen Mary, University of London (UK), has identified genetic variations on chromosome 6p21 and on chromosome 16q24. Their research is published online September 9 in Nature Genetics.

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Stopping colitis, STAT

Although the inflammatory bowel diseases – ulcerative colitis and Crohn’s disease – have distinct patterns of injury and inflammation, the existing therapies are quite similar and no therapies specifically target the Th2 immune response activated in ulcerative colitis.

The signaling molecule IL-13 (a key Th2 cytokine) has been implicated in the pathogenesis of the disease, but no group has demonstrated evidence of increased IL-13 signaling in colon tissues of patients with the disease.

Michael Rosen, assistant professor of pediatrics, and colleagues now show that STAT6, the key transcription factor activated by IL-13, is activated in colon tissue from pediatric patients recently diagnosed with ulcerative colitis.

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