Macrophage-Listeria interactions.
It is clear that the interaction between macrophages and the facultative intracellular bacterium Listeria monocytogenes is complex and dictated by the needs of both organisms. On the one hand, the invading pathogen has devised strategies to locate itself intracellularly in a site where host defense mechanisms are minimal; thus it escapes the phagosome and enters the cytoplasm, from which it travels to the next cell without exposing itself to the extracellular environment. On the other hand, the infected cell, potentially a highly efficient killer of microbes, is influenced by cytokines and other mediators, autocrine and exocrine, that enhance its ability to thwart the invader. Thus a macrophage, under the influence of at least IFN-gamma and TNF-alpha, can progress from being a nonlistericidal cell to one that can kill the intracellular organism. It probably does this by preventing escape of Listeria from the phagosome into the cytoplasm. The bacterium, retained in the phagosome, is killed by unknown mechanisms, which appear to be regulated by iron and may involve reactive nitrogen intermediates.
Campbell
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PA
National Jewish Center for Immunology and Respiratory Medicine, Denver, Colorado.
D000818:Animals; D016207:Cytokines / Q000276:immunology; D003602:Cytotoxicity, Immunologic; D006801:Humans; D007371:Interferon-gamma / Q000276:immunology; D008089:Listeria monocytogenes / Q000276:immunology* / Q000472:pathogenicity; D008088:Listeriosis / Q000209:etiology / Q000382:microbiology; D008264:Macrophages / Q000276:immunology* / Q000382:microbiology; D010587:Phagocytosis; D014409:Tumor Necrosis Factor-alpha / Q000276:immunology; D014774:Virulence
D016207:Cytokines; D014409:Tumor Necrosis Factor-alpha; D007371:Interferon-gamma