Journal
FRONTIERS IN BIOSCIENCE-LANDMARK
Volume 12, Issue -, Pages 2683-2692Publisher
FRONTIERS IN BIOSCIENCE INC
DOI: 10.2741/2364
Keywords
listeriolysin O; ROI; RNI; NOS2; phagosome maturation; cholesterol-dependent cytolysin; interferon-gamma; Rab5; lysosome; review
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Funding
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R01AI035950] Funding Source: NIH RePORTER
- NIAID NIH HHS [R01 AI035950-14, R01 AI035950, R0I AI 35950] Funding Source: Medline
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Macrophage activation often contributes to the strong immune response elicited upon infection. The ability of macrophages to become activated was discovered when sub-lethal primary infections of mice with the bacterium Listeria monocytogenes provided protection against secondary infections through non-humoral immunity. L. monocytogenes infect and propagate in macrophages by escaping the phagosome into the cytosol, where they avoid humoral immune mediators. Activated macrophages kill L. monocytogenes by blocking phagosomal escape. The timing of the antimicrobial activities within the phagosome is crucial to the outcome. In non-activated macrophages, bacterial factors generally prevail, and L. monocytogenes can escape from the vacuoles and grow within cytoplasm. Activated macrophages generate reactive oxygen or nitrogen intermediates early after bacterial uptake, which prevent the bacteria from escaping vacuoles into cytoplasm. The heterogeneity in the interactions between L. monocytogenes and the macrophage indicate a complex relationship between the host and the pathogen governed by chemistries that promote and inhibit escape from vacuoles. This review examines the mechanisms used by activated and non-activated macrophages to kill microbes, and how those mechanisms are employed against L. monocytogenes.
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