Jessica Sieff | December 10, 2018
In a new study published in the Journal of Experimental Medicine, scientists at the University of Notre Dame have discovered that the pathogen Mycobacterium tuberculosis (MTB) releases RNA into infected cells. This RNA stimulates the production of a compound known as interferon beta that appears to support the growth of the pathogen.
As part of the study the researchers found that mice lacking a key protein required for responding to foreign RNA and therefore required for interferon beta production were better able to control the MTB infection. The discovery was a surprise to the researchers, as interferon beta is essential to controlling several viral infections.
“The results suggest that our immune response to mycobacterial RNA is beneficial for the pathogen and bad for the host. It’s the total opposite of viral infections,” said Jeff Schorey, George B. Craig Jr. Professor in the Department of Biological Sciences at Notre Dame and co-author of the study. “This study gives us a better understanding of how the mycobacteria causes disease and what makes it the most successful pathogen in human history.”
MTB infections cause a battle between the immune response and the ability of the bacteria to circumvent that response — who wins the battle determines the body’s ability to control the infection. Schorey and Yong Cheng, a research assistant professor at Notre Dame, set out to determine how mycobacteria RNA could be affecting the host response. What they found was that by releasing RNA, the bacteria set off a chain reaction inside the macrophage, a cell type of the immune system — resulting in a mechanism that benefits the survival of MTB through the production of interferon beta.
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