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A recently identified path of inflammation once thought to be wholly independent of other inflammatory systems has now been linked to another major pathway. The findings by neuroscientists at Johns Hopkins are likely to point scientists to novel drugs that significantly reduce the risks of taking COX-2 inhibitor pain relievers, the investigators report.

In a paper published in the Dec. 23 issue of Science, a Johns Hopkins team led by Solomon H. Snyder, M.D., said the iNOS (inducible nitric oxide synthase)-based inflammation pathway has now been found to cross-link with the more well-known COX-2 pathway that is the target of COX-2 inhibitor drugs such as Vioxx. Until now, these two major inflammatory mechanisms were assumed to be unrelated and independent of each other, the researchers say.

"The fundamental significance of this work is that it demonstrates a totally unsuspected connection between the two most important inflammatory systems in the body," says Snyder, professor and director of neuroscience in Johns Hopkins' Institute for Basic Biomedical Sciences. "The therapeutic significance is that drugs which block the binding of iNOS and COX-2 might represent novel anti-inflammatory agents or reduce the dosage needed and side effects of this family of drugs."

COX-2 is an enzyme that makes prostaglandins, molecules that cause inflammation and pain. iNOS is an enzyme that makes NO (nitric oxide), a molecule that acts as a signal for a variety of cellular functions throughout the body, including the triggering of inflammation, dilating of blood vessels and penile erection.

The site on the iNOS protein that binds to COX-2 is close to the active or business end of the iNOS, the researchers found. As a result, it should be possible to design drugs that do double duty by inhibiting iNOS while also blocking iNOS binding to COX-2. This would decrease the formation of both NO and prostaglandins, Snyder said.

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Contact: Joanna Downer
jdowner1@jhmi.edu
410-614-5105
Johns Hopkins Medical Institutions
22-Dec-2005

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