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Mechanism that leads to inflammatory diseases discovered

March 15th, 2012
by Tania

The mechanism in cells that leads to inflammatory diseases has been discovered by researchers, which could lead to advances in the treatment of rheumatoid arthritis, Type 2 diabetes and numerous other chronic diseases.

Cedars-Sinai researchers have released the study to the peer-reviewed journal Immunity, demonstrating how they have revealed how an inflammatory molecule is produced in the body. The study was funded by the National Institutes of Health, and it is the first time the mechanism that leads to the production of the molecule interleukin-1beta has been identified. This is a major contributor to inflammation, which lies at the root of many serious health conditions, including atherosclerotic heart disease and some types of strokes.

Currently, drugs are used to block this molecule’s action after it is secreted by cells. However, the new research could lead to the development of treatments that would prevent the body from producing it at all.

Dr. Moshe Arditi, executive vice chair of research in the Department of Pediatrics and director of the Division of Pediatric Infectious Diseases and Immunology said: "If we understand how this molecule is made in the body, we may be able to block it before it is produced."

"Until now, this was the missing piece of the puzzle."

The researchers found that  damaged mitochondrial DNA activate specific proteins within dying cells, triggering the release of interleukin-1beta. This molecule can be a significant contributor to major inflammatory diseases. Three of which alone, in atherosclerosis, Type 2 diabetes and rheumatoid arthritis, affect hundreds of millions of people worldwide.

Arditi is planning further studies to build on the findings, and continued to emphasise the impact the study could have on a wide range of inflammatory diseases, particularly those in the early stages. Further research will open up a wealth of new avenues that will be explored using this research as their basis.

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