Discovery of a 'molecular switch' may lead to new ways of treating infection, including MRSA

Main Category: MRSA / Drug Resistance
Article Date: 28 Apr 2005 - 0:00 PDT

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The discovery of a 'molecular switch' could lead to new ways of treating infections such as MRSA, and inflammatory diseases like arthritis.

According to research published today in Nature, the team from Imperial College London and the University of California, San Diego, have identified an enzyme called IKKá, which can act as a 'brake' on an immune cell pathway responsible for regulating the body's response to infection and inflammation.

By inhibiting IKKá activity the researchers were able to increase the body's ability to fight off infection, but at the same time also increased the body's inflammatory response. They also found that IKKa inhibits activation of immune cells, and inhibits inflammation, a discovery which could lead to new ways of treating diseases such as arthritis.

Dr Toby Lawrence, a Wellcome Trust International Research Fellow from Imperial College London, based at the Kennedy Institute of Rheumatology, and lead author of the research, says: "The identification of this 'double-edged sword' could be of huge importance in how we deal with a number of major health issues, including MRSA. With antibacterial resistance on the rise, this development could provide doctors with a new way to stop infections without resorting to a cocktail of antibiotics.

"Although this is only a first step, the discovery could also help arthritis sufferers. By increasing IKKa activity we may be able to stop inflammation, and possibly develop a new treatment."

The team investigated the role of IKKá in inflammation and immunity by comparing the response of mice with a defective IKKá enzyme, compared to normal mice, when exposed to the pathogen Streptococcus. In the mice without IKKá, they found significantly increased killing of bacteria in sepsis and pneumonia, but found that inflammation was higher than the normal mice. This result led the team to believe that IKKá was a stop signal to limit the inflammatory response.

Contact: Tony Stephenson
at.stephenson@imperial.ac.uk
44-20-7594-6712
Imperial College London
http://www.imperial.ac.uk/press

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