Targeting an enzyme called cGAS could be a promising pathway for developing much-needed new immunity-based therapies aimed at treating tuberculosis infection, according to a new study from the University of Texas Southwestern Medical Center.
The researchers looked at mice infected with Mycobacterium tuberculosis — the strain of bacteria that leads to tuberculosis infection — and reported that animals without the enzyme were much more vulnerable to TB than those with normal levels of cGAS.
"Based on this outcome, we believe that modulating cGAS activity could be a novel approach to therapy. There remains a dire need for new therapies against tuberculosis, and thus identifying pathways to stop the pathogen is of vital importance," Dr. Michael Shiloh, assistant professor of internal medicine and microbiology at UT Southwestern and co-senior author of the study, said in a statement.
When TB is detected in the system by the cGAS enzyme, a series of events is triggered. The body will produce compounds that rally the production of cells to initiate defense mechanisms against the bacteria, according to the study. Understanding this cascade of events also has potential use as a diagnostic biomarker for measuring therapeutic response to newly developed TB treatments.
TB is an airborne bacterium and is second only to HIV/AIDS as the greatest killer worldwide due to a single infectious agent, according to the World Health Organization. The CDC estimates that about 4 percent of Americans are latent carriers of the virus, and TB resistance to the most commonly used and potent drugs is rising.
More articles on infection control:
10 clinical research findings to know this week
Re-engineered antibiotic may combat resistant bacteria
Researchers work to develop treatment plans for C. diff: 5 predictors