Researchers find clues to treating tuberculosis in enzyme
Colorado State University researchers say they have discovered an enzyme that could help in the treatment of tuberculosis, one of the world's most deadly diseases.
Currently, about one-third of the entire global population is infected with tuberculosis. In 2010, about 1.4 million people died of tuberculosis or illnesses related to the disease, and 9 million people became ill with tuberculosis, according to the Centers for Disease Control.
While tuberculosis is more common in other countries, the CDC says more than 11,000 new cases were reported in the United States in 2010.
At CSU, researchers have found an enzyme that is critical to the survival and replication of the bacterial pathogen that causes tuberculosis. The enzyme could become a key target for new drugs that may halt manifestation of tuberculosis and potentially cut the current treatment regimen of multiple antibiotics given daily for at least six months, CSU says.
The key enzyme is present in both replicating and non-replicating strains of the bacteria, including resistant strains. That's key because non-replicating bacteria are much more difficult to kill with antibiotics, which is one reason treatments for tuberculosis are so long-lasting.
"Another interesting observation that arose from our work is that this enzyme — known as FBA-tb — is on the surface of the bacterium. Because it is on the surface, it has the ability to interact with a human substance called plasminogen, which plays a key role in our immune response," said Mary Jackson, an associate professor in CSU's Department of Microbiology, Immunology and Pathology.
Jackson works in the Mycobacterial Research Laboratories.
"This finding suggests that the bacteria that cause tuberculosis may use this enzyme to manipulate our immune system that spread tuberculosis throughout our body," she said. "We are looking into that theory now."
The research discovery was published recently in the issue of the Journal of Biological Chemistry.
By Monte Whaley
Denverpost.com