A hallmark of pathogenic mycobacteria is their ability to block phagosome maturation. The vacuole that pathogenic mycobacteria reside within can be characterized by limited proteolytic activity, lowered acidity and lack of specific maturation markers such as Rab7, syntaxin-6 and LAMP-1.
Although we are beginning to appreciate how pathogenic mycobacteria block phagosome maturation, there still remain gaps in our understanding. We have been conducting studies to address TLR2 role in regulating mycobacterial phagosome maturation based on published data indicating that TLR2 and -4 promote trafficking of phagocytosed bacteria to a phagolysosomal compartment. We did not observe any differences between murine bone marrow-derived macrophages isolated from TLR2^-/- or wild type mice in the phagocytosis or trafficking of live Mycobacterium avium. However, phagosomes containing heat-killed M. avium showed delayed acidification in TLR2^-/- compared to wild type macrophages and a lack of lysosomal associated membrane protein-1 staining in the knockout macrophages. The belated phagosome acidification seen in TLR2^-/- macrophages may be due to an observed delay in the proton ATPase recruitment.
Pathogenic Mycobacteria are known to block mobilization of calcium from intracellular compartments leading to inhibition of Ca²⁺ signaling, vital for the process of phagosome maturation. Moreover, it has recently been shown that TLR2 can activate these signaling pathways. We have analyzed the role of TLR2 receptor in calcium-dependent signaling pathway in context of phagosome maturation.
We are continuing to characterize the signaling pathways that may originate from TLR2 receptor and regulate maturation of phagosomes containing dead M. avium 101. Obtained results should help in understanding the role of this receptor in controlling of mycobacterial infections.

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