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FP6

TB-MACS — Result In Brief

Project ID: 37732
Funded under: FP6-LIFESCIHEALTH

Disarming the TB bacterium

During infection, the bacterium responsible for tuberculosis (TB) exhibits some amazing control features of the host cell contents. A European research project has identified and isolated the genes responsible for these survival mechanisms in a bid to develop new TB drugs and vaccines.
Disarming the TB bacterium
Mycobacterium tuberculosis (M.tuberculosis), the cause of TB, is still a major threat to human health being responsible for around two million deaths every year. Current control measures are inadequate and the EU-funded TB-MACS project aimed to tackle this deficiency with research into genes responsible for the pathogen's successful multiplication in the host cell.

Central to the success of M.tuberculosis is its ability to survive in the phagosome of its host. A cellular compartment where pathogenic microorganisms are normally killed and digested, the phagosome normally breaks down its contents after fusion with another cell body, the lysosome, to form the phagolysosome.

The infectious cycle of M.tuberculosis relies on the bacterium being able to inhibit the acidification process in the phagosome and prevents formation of the phagolysosome. Scientists in the TB-MACS consortium investigated M.tuberculosis mutants that were unable to inhibit the acidification process and/or the formation of the phagolysosome.

TB-MACS researchers used novel microarray-based genetic screens to identify the mutants. The variants were then isolated and characterised with respect to trafficking of intracellular products and growth in the human phagosome. TB-MACS successfully examined the mutant transcription gear and proteins to identify bacterial products that are essential for successful infection.

Identification of the M.tuberculosis survival kit can be used for new drug therapies. Mutant genes can be used to develop attenuated or weakened strains for vaccines.

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