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Compounds That may Provide Promising Therapies for Cystic Fibrosis Identified

by VR Sreeraman on Mar 20 2008 8:01 PM

University of Toronto scientists say that they have identified several compounds that may pave the way for developing innovative therapies against cystic fibrosis, a serious disease that causes blockages in the lungs and other organs like the liver and the pancreas.

Professor Igor Stagljar, who led the research project, says that one of the compounds identified by his team, exosin, has been found to significantly inhibited infections in mammalian cells, suggesting that it has the potential to improve the effectiveness of antibiotics in the treatment of chronic and acute bacterial respiratory infections in cystic fibrosis patients.

Previous studies had suggested that the onset of certain chronic or deadly infections in cystic fibrosis patients could be prevented by administering them early antibiotic treatment.

However, the current availability of antibiotics against Pseudomonas aeruginosa, a pathogen that may cause a host of infections, is limited. Moreover, the pathogen has started to show signs of drug resistence these days.

Professor Stagljar now says that he and his colleagues have identified several drugs that block a key protein that underpins Pseudomonas aeruginosa's ability to spread infections, called exoenzymeS (ExoS).

"These studies created a road map to the rational design of more potent, highly selective inhibitors against other similar toxins using a totally novel yeast-based approach," says lead author Professor Stagljar.

He says that his research may also serve as a model for future therapies against the HIV virus.

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“This innovative approach is an important advance, not only for the value it may have in cystic fibrosis treatment, but also because this technique could be used to design novel therapies for any bacterial pathogen as well as the HIV virus,” he adds.

Professor Stagljar and his colleagues are gearing up to test their inhibitors on an animal model of cystic fibrosis.

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Source-ANI
SRM/M


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