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Infectious disease


G protein-coupled receptor 109A (GPR109A; HM74A)

A study in macrophages and mice suggests inhibiting GPR109A could help treat tuberculosis. In Mycobacterium tuberculosis-infected macrophages, small interfering RNA knockdown of the host protein GPR109A decreased the accumulation of lipid bodies, which are a nutrient source for the bacteria, compared with no knockdown. In mice infected with M. tuberculosis, the GPR109A inhibitor mepenzolate bromide decreased pathogen loads in the lung, liver and spleen compared with vehicle. Next steps could include developing GPR109A inhibitors with better pharmacokinetics and testing the longer-term effects of inhibiting GPR109A in animal models of M. tuberculosis infection.

SciBX 5(49); doi:10.1038/scibx.2012.1287
Published online Dec. 20, 2012

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Singh, V. et al. Cell Host Microbe; published online Nov. 15, 2012;
Contact: Kanury V.S. Rao, International Centre for Genetic Engineering and Biotechnology, New Delhi, India