Cyclin-dependent kinase inhibitors: The latest anti-inflammatory
By University of Edinburgh
Sep 4, 2006, 16:41

People who suffer from inflammatory conditions such as chronic diseases of the lung, joints and other organs could benefit from a new discovery by scientists at the University of Edinburgh. A new study in Nature Medicine journal shows that certain drugs, already being tested as cancer treatments, can dramatically reduce tissue inflammation.

The researchers have found that certain non-biological drugs, known as CDK inhibitors, can knock out the inflammatory cells which cause the tissue damage and scarring that leads to organ failure and joint pain. These drugs trigger a process of cell 'suicide' called apoptosis in which the inflammatory cells, called neutrophils, destroy themselves before being removed by scavenger cells, called macrophages.

The Edinburgh scientists have spent years devising ways of inducing apoptosis in specific inflammatory cells while, in parallel, driving macrophages to clear the resultant apoptotic cells more rapidly. Now they have shown that CDK inhibitors, like Roscovitine which is already being tested in human cancer are capable of inducing neutrophil apoptosis 'in the test-tube'. Significantly, laboratory tests now suggest that they also reduce inflammation in models of rheumatoid arthritis and a devastating, currently untreatable, lung disease called fibrosing alveolitis.

Professor Chris Haslett, Head of the Queen's Medical Research Institute at the University of Edinburgh, expects the study to lead to trials of these drugs in human inflammatory diseases. Professors Adriano Rossi and Haslett, who have led this new study with other colleagues from the QMRI, said: "This study offers new hope for patients with severe inflammatory diseases. Specific treatment for such conditions is poor, and the use of steroids is fraught with potential difficulties. We have adopted a different strategy by using non-biological treatments, but this study needs urgently to be translated into trials and we are now seeking major funding to research further how these drugs work."

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