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Protease-inhibitor cocktail protects, increases anti-microbial action of promising new peptide

BUFFALO, N.Y. -- The anti-microbial activity of promising peptides shown in laboratory studies to kill several medically important fungi, some of which are resistant to current drugs, can be enhanced further by protecting the peptides from enzymes programmed to destroy them, University at Buffalo oral biologists have found.

A protease inhibitor cocktail containing compounds that inactivate the enzymes that normally would degrade the small pieces of protein enabled the potential treatments for oral infections to more than double their anti-microbial action, results showed.

Guo-xian Wei, D.D.S., postdoctoral associate in the laboratory of Libuse Bobek, Ph.D., professor of oral biology in UB's School of Dental Medicine, reported the study findings today (March 11, 2004) at the International Association of Dental Research meeting in Hawaii.

One peptide in particular, called MUC7 12-mer, a piece of a larger, naturally occurring human salivary mucin molecule, has shown particular promise for treating drug-resistant fungal strains, Wei said.

Only a few drugs are available to treat these infections, and some fungal organisms already are resistant, presenting a particular problem for patients with depressed immune systems, such as those with HIV/AIDS, organ-transplant patients and chemotherapy patients.

In earlier research in Bobek's laboratory, MUC7 12-mer killed fungal agents that cause the most common opportunistic infections that threaten these patients -- candidiasis and cryptococcosis. In addition, the peptide was active in very low concentrations, reducing the likelihood of adverse reactions.

However, when the UB researchers tested MUC7 12-mer in saliva, its potency decreased considerably. They theorized that enzymes, or proteases, in the saliva were breaking down the peptide. To test their theory, they exposed the microbes to the peptide in the presence of saliva and a commercially available protease inhibitor cocktail.

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Contact: Lois Baker
ljbaker@buffalo.edu
716-645-5000 x1417
University at Buffalo
11-Mar-2004


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