Natural Resistance to Listeria Monocytogenes as a Function of Macrophage Inflammatory Response
The accumulation and mobilization of mononuclear phagocytes to foci of infection provide a vital source of effector cells for host defense against intracellular pathogens. For example, during the course of infection in mice with Listeria monocytogenes, the accumulation of inflammatory macrophages has been shown to be critical in preventing fulminant bacterial growth in the infected organs before the appearance of sensitized T-cells and subsequent activation of macrophages (1,2). The recruitment of adequate numbers of inflammatory macrophages may, therefore, be related to the level of genetically-determined host resistance to infection with Listeria. The level of resistance in inbred mice is genetically controlled by a single, dominant, non H-2 linked autosomal gene which has been named the Lr gene (3,4). In surveying various inbred strains of mice which can be distinguished on the basis of the presence or absence of the resistant allele at the Lr gene locus, we have found differences in the number of macrophages which accumulate in the peritoneal cavity following intraperitoneal (ip) treatment with thioglycollate.
KeywordsListeria Monocytogenes Resistant Allele Mononuclear Phagocyte System Inflammatory Macrophage Chemotactic Responsiveness
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