Which glycolipid inhibits phago-lysosome fusion in Mycobacterium tuberculosis?

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Multiple Choice

Which glycolipid inhibits phago-lysosome fusion in Mycobacterium tuberculosis?

Blocking phagosome-lysosome fusion inside macrophages is a key survival strategy for Mycobacterium tuberculosis. Sulfatides, sulfated galactosylceramides on the mycobacterial surface, disrupt the host’s phagosome maturation process. This interference prevents the phagosome from fusing with lysosomes and becoming a degradative, acidic compartment, so the bacteria can persist in a relatively safe intracellular niche. Trehalose dimycolate (cord factor) is another virulence lipid that contributes to the bacterium’s effects on the host, notably granuloma formation and cytotoxic responses, but the specific lipid class most consistently linked to inhibiting phagosome-lysosome fusion is sulfatides. Catalase-peroxidase (KatG) is an enzyme involved in activating certain drugs and defending against oxidative stress, not a glycolipid. Mycolic acid is a major cell-wall lipid that affects permeability and immune interactions in general, but it is not the primary factor cited for blocking phagosome-lysosome fusion.

Blocking phagosome-lysosome fusion inside macrophages is a key survival strategy for Mycobacterium tuberculosis. Sulfatides, sulfated galactosylceramides on the mycobacterial surface, disrupt the host’s phagosome maturation process. This interference prevents the phagosome from fusing with lysosomes and becoming a degradative, acidic compartment, so the bacteria can persist in a relatively safe intracellular niche.

Trehalose dimycolate (cord factor) is another virulence lipid that contributes to the bacterium’s effects on the host, notably granuloma formation and cytotoxic responses, but the specific lipid class most consistently linked to inhibiting phagosome-lysosome fusion is sulfatides. Catalase-peroxidase (KatG) is an enzyme involved in activating certain drugs and defending against oxidative stress, not a glycolipid. Mycolic acid is a major cell-wall lipid that affects permeability and immune interactions in general, but it is not the primary factor cited for blocking phagosome-lysosome fusion.

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