Researchers discover new paths for asthma treatment

Researchers at the University of Newcastle and the Cooperative Research Centre (CRC) for Asthma and Airways have made a major breakthrough that has the potential to revolutionise the treatment of asthma and, potentially, other inflammatory diseases.

Professor Paul Foster, Associate Professor Joerg Mattes and a team of young CRC scientists in the Hunter have discovered, for the first time, a way to stop inflammation, the main cause of asthma and other chronic diseases, by blocking malfunctioning microRNA molecules.

MicroRNA molecules regulate protein production in human cells. When the molecules malfunction they cause an imbalance in protein levels, leading to an inflammation in the body. This inflammation can manifest as asthma, rheumatoid arthritis or a number of other conditions.

“Based on the understanding that malfunctioning microRNA molecules may lead to asthma or other types of inflammation, our research team has been looking at ways to inhibit their function,” Professor Foster said.

“The research team has established in an asthma model, for the first time, that the effect of a malfunctioning microRNA can be blocked with a specific chemical (antagomir) treatment.” Current therapies use inhaled steroids to suppress the inflammatory response and relieve asthma symptoms. Long-term use of steroids can be harmful.

“Our major discovery opens up a number of exciting pathways, using a direct intervention at the molecular level to treat inflammatory conditions such as asthma and, potentially, other inflammatory diseases such as rheumatoid arthritis,” he said.

“Essentially we are developing new possibilities to treat the cause rather than just the symptoms.” The next step is to replicate the testing with human tissue.

The research has been published this month in one of the world’s most respected journals, Proceedings of the National Academy of Science, USA. It was funded by the CRC for Asthma and Airways, with support by the National Health and Medical Research Council.