jer

Here's an article I read the other day. Looks promising to me.

Yale team finds gene linked to bowel ills
Abram Katz, Register Science Editor

10/30/2006
Email to a friendPrinter-friendly
A team of Yale scientists has identified a gene closely associated with inflammatory bowel diseases, a group of painful and restrictive disorders that affects 1 million Americans.


The finding is considered a significant advance in the genetics of inflammatory bowel disease, which includes Crohn’s disease, ulcerative colitis and irritable bowel syndrome.


These chronic disorders cause abdominal pain and cramps, diarrhea, gastrointestinal bleeding and other symptoms.

Dr. Judy H. Cho, associate professor of medicine and genetics in the Yale School of Medicine and senior author of the study, which appears on the Science Express Web site, said researchers also discovered a mutation of the gene that protects carriers against inflammatory bowel disease.

Eventually, the research could lead to better, more individualized treatments for inflammatory bowel disease, she said. The disorders do not affect life expectancy, but can ruin the quality of life, Cho said.

The study was financed by the National Institute of Diabetes and Digestive and Kidney Diseases, a section of the National Institutes of Health.

Dr. Stephen P. James, director of NIDDK, said, "This important discovery not only offers new hope for better therapies for patients with Crohn’s disease, it also highlights the promise of the human genome project and subsequent investments by the NIH in large-scale, collaborative projects."

Cho and colleagues compared 300,000 genetic markers in families with and without inflammatory bowel disease.

Cho found the gene for interleukin-23, as well as a mutated version of the gene that confers defense against inflammatory bowel disease. Efforts to control inflammatory bowel disease have concentrated on the IL-23 pathway, but the underlying genetics were not clear.

IL-23 is one of dozens of small proteins produced by the immune system and that regulate immunity and inflammation. IL-23 is known to activate inflammation in digestive organs.

This gene is "normal" in that it is carried by a large majority of the population, Cho said. IL-23 connects with receptors on cell surfaces, which trigger the cells to issue a chemical call for additional defensive proteins that repel invading microbes through inflammation.

The discovered mutation is in the IL-23 receptor. It is unable to recognize IL-23 and consequently does not respond to the interleukin cytokine.

About one in 1,000 Americans develop inflammatory bowel disease. It is especially prevalent in families of European Jews. One out of six to seven Caucasians carry a copy of the protective mutation, Cho said.

Cho said the IL-23 gene is probably involved in other inflammatory disorders, such as psoriasis.

Possible treatments could include molecules that imitate the receptor mutation by blocking the receptors for IL-23. Research elsewhere has shown that antibodies apparently can interfere with cytokine synthesis.

Since inflammation is one of the body’s main defenses against infection, a drug would have to selectively muffle only a few responses, Cho said. Blocking IL-23 otherwise might encourage infections.

Cho and co-authors represent Yale’s membership in the IBD Consortium, which includes Cedars-Sinai Medical Center in Los Angeles, the University of Chicago, Johns Hopkins University, Université de Montréal, the University of Pittsburgh and the University of Toronto.


--------------------------------------------------------------------------------
Abram Katz can be reached at akatz@nhregister.com or 789-5719.





©New Haven Register 2006