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*
Max-Planck Institute for Infection Biology, Department of Immunology, Berlin, Germany;
Free University-Berlin, Department of Biology, Chemistry, and Pharmacy, Berlin, Germany; and
Department of Microbiology, Colorado State University, Fort Collins, CO 80523
Pathogenic mycobacteria are able to survive and proliferate in
phagosomes within host macrophages (M
). This capability has been
attributed in part to their cell wall, which consists of various unique
lipids. Some of these are important in the host-pathogen interaction,
such as resistance against microbicidal effector mechanisms and
modulation of host cell functions, and/or are presented as Ags to T
cells. Here we show that two lipids are released from the mycobacterial
cell wall within the phagosome of infected M and transported out of
this compartment into intracellular vesicles. One of these lipids was
identified as lysocardiolipin. Lysocardiolipin was generated through
cleavage of mycobacterial cardiolipin by a Ca2+-independent
phospholipase A2 present in M lysosomes. This result
indicates that lysosomal host cell enzymes can interact with released
mycobacterial lipids to generate new products with a different
intracellular distribution. This represents a novel pathway for the
modification of bacterial lipid Ags.
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