Tens of millions of individuals worldwide suffer from type 2 diabetes, rheumatoid arthritis, as well as several other chronic diseases. Now a study funded by the National Institutes of Health reveals that Cedars-Sinai researchers have, for the first time, identified the mechanism that causes the production of the molecule interleukin-1beta. According to the researchers, this finding could result in advances in treating inflammatory diseases.
The study will appear in the March print edition of the peer-reviewed journal Immunity.
The mechanism the team discovered plays a significant role in inflammation. Inflammation lies at the root of several serious health conditions, such as some types of strokes and cardiovascular disease.
At present, medications are designed to prevent interleukin-1beta’s action after it is secreted by cells. The teams findings may result in the development of treatments that would inhibit this molecule from being produced in the body, resulting in more effective therapies and medications for inflammatory diseases.
Dr. Moshe Arditi, study author, executive vice chair of research in the Department of Pediatrics, director of the Division of Pediatric Infectious Diseases and Immunology, and director of Cedars-Sinai’s Infectious and Immunologic Diseases Research Center, said:
“If we understand how this molecule is made in the body, we may be able to block it before it is produce. Until now, this was the missing piece of the puzzle.”
Furthermore, the researchers found that within dying cells, damaged mitochondrial DNA trigger specific proteins which activate the release of interleukin-1beta. Earlier studies have demonstrated that when interleukin-1beta is over-secreted by cells, the molecule can be a considerable contributor to major inflammatory diseases.
An estimated 100 million individuals in the U.S., are affected by three of diseases alone – type 2 diabetes, rheumatoid arthritis, and atherosclerosis.
The team plan to conduct additional studies, in order to build on the findings from this study.
Dr. Leon Fine, Cedars-Sinai’s vice dean of research and chair of biomedical sciences, explained:
“The discovery by Arditi and colleagues has great potential to impact a wide range of inflammatory diseases, particularly in their early stages where an intervention could prevent more severe and debilitating ravages of such diseases. This discovery, at last, may open the door to such therapy.”
As well as the researchers from Cedars-Sinai, other research teams involved in the investigation include UCLA ‘s David Geffen School of Medicine, UC Merced’s Health Sciences Research Institute and School of Natural Sciences; UC Riverside’s Department of Chemistry and the University of Massachusetts Medical School’s Department of Medicine.
Written by Grace Rattue