engleski

Divergence in the intracellular life style of Legionella longeachae from Legionella pneumophila

Legionella species are responsible for a severe pneumonia known as Legionnaires' disease. Legionella pneumophila is the predominant couse of Legionnaires' disease in the United States and in Europe in contrast to L. longbeachae which is the leading cause of the disease in Australia, and is an emarging pathogen in the United States. The ability of L. pneumophila to replicate intracellularly is triggered at the post-exponential phase along with expression of other virulence traits, such as motility. We show that robust inracellular replication of L. longbeachae is independent of the growth phase. Within alveolar macrophages, L. pneumophila replicates in a phagosome that excludes early and late endocytic markers and is surrounded by the rough endoplasmic reticulum (RER). Here we show the L. longbeachae phagosome co-localizes with the early endosomal marker EEA1 and the late endosomal markers LAMP-2 and Mannose-6-Phosphate Receptor (M6PR), and is surrounded by the RER. The L. longbeachae phagosome excludes the vacuolar ATPase proton pump (vATPase), the lysosomal protease cathepsin D, and the lysosomal tracer Texas red ovalbumin (TROV). We show that intracellular proliferation of L. longbeachae occurs in LAMP-2 positive pahgosomes that axquire the RER. During late stages of infection, L. longbeachae escape into the cytoplasm, prior to lysis of the macrophage, similar to L. pneumophila. Despite the different trafficking of L. longbeachae and L. pneumophila, both can replicate in communal phagosomes harboring both species. In addition, the L. pneumophila dotA mutant is rescued for intracellular replication if it co-inhibits the phagosome with L. longbeachae. Our date indicate a unique trafficking of L. longbeachae compared to other intracellular pathogens, and divergence in the intracellular life style of L. longbeachae from L. pneumophila.

endocytic markers; egress; legionnaire's disease

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