ITHACA, N.Y., March 30 (UPI) — A U.S. medical scientist studying factors that trigger latent tuberculosis says his findings might lead to innovative strategies for treating the disease.
Cornell University Professor David Russell and his team demonstrated TB-causing bacteria are able to hijack fat metabolism in the host to drive the progression of the disease. They showed Mycobacterium tuberculosis is able to stimulate macrophages — the immune cells the bacterium infects — to accumulate fat droplets, turning them into “foamy” cells. That cellular transformation, the researchers said, can trigger a reawakening of the TB infection from its latent state.
Russell said the findings suggests lipids in the newly formed foamy cell are then expelled into the cellular environment, allowing the infectious bacteria to leak into the airways where they can progressively destroy lung tissue.
“If our model is correct, it has huge implications for vaccines and chemotherapy programs,” Russell said. “A more detailed knowledge of the bacterium’s life cycle and its host interactions will allow us to spot new targets for drugs, opening up new possibilities for treatment.”
The study was presented last week in Edinburgh, Scotland, during a meeting of the Society for General Microbiology.
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