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


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Under embargo for

18.00 BST/13.00 EST
Wednesday 27 April 2005

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 IKKa, which can act as a brake on an immune cell pathway responsible for regulating the bodys response to infection and inflammation.

By inhibiting IKKa activity the researchers were able to increase the bodys 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 IKKa in inflammation and immunity by comparing the response of mice with a defective IKKa enzyme, compared to normal mice, when exposed to the pathogen Streptococcus. In the mice without IKKa, 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 IKKa was a stop signal to limit the inflammatory response.

For further information please contact (media only):

Tony Stephenson
Imperial College London Press Office
Tel: +44 (0)20 7594 6712
Mobile: +44 (0)7753 739766
E-mail: at.stephenson@imperial.ac.uk

Notes to editors:

IKKa limits macrophage (NF)-kB activation and contributes to the resolution of inflammation, Nature 3491, 27 April 2005.

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