University of Maryland researchers have discovered how the bacterium associated with tuberculosis suppresses immune defenses in infected human cells, which can exacerbate the infection.
This new finding, published yesterday in the journal PLOS Pathogens, may point to an effective target for a gene-based treatment or preventative therapy for tuberculosis, which sickens about 10 million people and kills 1 million to 2 million people annually, according to the World Health Organization. Available treatments are only 85% effective, and multidrug-resistant forms of tuberculosis pose a public health threat in many parts of the world.
“In order to develop novel therapeutic targets, an understanding of the molecular mechanisms of how bacterial proteins interact with human cells is essential,” said Volker Briken, a professor of cell biology and molecular genetics at UMD and the senior author of the study.
Briken and his team, led by postdoctoral fellow and lead author of the study Shivangi Rastogi, made their discovery by infecting a type of white blood cell called a macrophage with either Mtb—the bacterium that causes tuberculosis—or a nonvirulent bacterium and observing the cell’s response.
The researchers found that a complex of proteins called the inflammasome was dramatically limited in cells infected with Mtb, but not in those infected with the non-virulent bacteria. The inflammasome surveys a cell’s interior for pathogens and then signals the cell to launch an immune response.
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