期刊
INFECTION AND IMMUNITY
卷 73, 期 5, 页码 3166-3171出版社
AMER SOC MICROBIOLOGY
DOI: 10.1128/IAI.73.5.3166-3171.2005
关键词
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资金
- NIAID NIH HHS [R21AI038410-06A1, R01 AI043965, R01AI43965] Funding Source: Medline
Legionella pneumophila is an intracellular pathogen that modulates the biogenesis of its phagosome to evade endocytic vesicle traffic. The Legionella-containing phagosome (LCP) does not acquire any endocytic markers and is remodeled by the endoplasmic reticulum during early stages. Here we show that intracellular replication of L. pneumophila is inhibited in gamma interferon (IFN-gamma)-activated, bone marrow-derived mouse macrophages and IFN-gamma-activated, human monocyte-derived macrophages in a dose-dependent manner. This inhibition of intracellular replication is associated with the maturation of the LCP into a phagolysosome, as documented by the acquisition of LAMP-2, cathepsin D, and lysosomal tracer Texas Red ovalbumin, and with the failure of the LCP to be remodeled by the rough endoplasmic reticulum. We conclude that IFN-gamma-activated macrophages override the ability of L. pneumophila to evade endocytic fusion and that the LCP is processed through the default endosomal-lysosomal degradation pathway.
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