Researchers are aiming to tackle diseases that affect millions -- such as asthma, blindness and clogged arteries -- by jamming 'sat nav'-like signals that drive the body to damage itself.
Dr James Pease, of Imperial College London, and colleagues are investigating how new 'blocker' drugs might be used to treat inflammatory diseases.
Dr Pease will talk about the progress and potential of his work to fellow researchers on December 15 at The British Pharmacological Society's Winter Meeting, during a special symposium.
He is currently working to understand how a specific protein called CCR3 functions -- and how newly developed drugs can be used to jam its communications.
During his presentation, Dr Pease will look at the potential for this approach to be used in the treatment of a variety of inflammatory disorders, including atherosclerosis and age-related macular degeneration.
He said: "The CCR3 protein has been likened to a 'sat nav' device that sits on the surface of white blood cells called leukocytes. The way leukocytes move around the body is controlled by proteins called chemokines, which are particularly generated during inflammation. Once chemokines have 'recruited' leukocytes to tissues in the body, the leukocytes are instructed to carry out several functions including the destruction of invading micro-organisms like bacteria. But the flip side of this is that inadvertent or excessive production of chemokines is responsible for the tissue damage observed in diseases such as asthma."
The CCR3 'sat nav' protein sits on the surface of the leukocyte, detects the chemokine signal and instructs the cell to move in the direction of the signal. Scientists already know it is feasible to use prototype drugs to jam the CCR3 signal that directs leukocytes to the asthmatic lung.
These drugs work by attaching themselves to CCR3 and disabling its 'sat nav' function.
Dr Pease says that while his group's research is still at a fairly early stage and there are significant hurdles to be overcome, their on-going work has given them a good idea of how CCR3 blocking works -- and could aid the design of future therapies.
He added: "We have recently found a naturally occurring mutant CCR3 which has lost its 'sat nav' function. This suggests jamming the communication ability of normal CCR3 proteins is a feasible proposition.
"One major problem faced by researchers is that the human CCR3 is significantly different from the CCR3 in rats or mice, so all possible CCR3 blockers have to be assessed on human cells, which has made progress much slower.
"There is still much work to be done, and although CCR3-blocking drugs described to-date have yet to prove successful in the clinic, we are excited by the potential for these drugs in the treatment of a variety of diseases, particularly asthma.
"The prospect of another class of anti-inflammatory drugs without the well-known side effects of the aspirin-like drugs or the steroids is what drives this research in academic labs and in the pharmaceutical industry."
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