| Summary: | <p>Abstract</p> <p>Background</p> <p><it>Cryptococcus neoformans </it>is an encapsulated yeast that is a facultative intracellular pathogen. The interaction between macrophages and <it>C. neoformans </it>is critical for extrapulmonary dissemination of this pathogenic yeast. <it>C. neoformans </it>can either lyse macrophages or escape from within them through a process known as phagosomal extrusion. However, most studies of intracellular pathogenesis have been made with mouse cells and their relevance to human infection is uncertain. In this study we extended studies of <it>C. neoformans</it>-macrophage cellular interaction/s to human peripheral blood monocytes.</p> <p>Results</p> <p>This study demonstrated that <it>C. neoformans </it>can shed polysaccharide within human monocytes, spread from cell to cell, and be extruded from them. Furthermore, human monocytes responded to ingestion of <it>C. neoformans </it>with cell cycle progression from G1 to S.</p> <p>Conclusion</p> <p>Similarities between mouse and human cells support the suitability of mouse cells for the study of intracellular pathogenesis mechanisms. Given that these hosts diverged over 70 million years ago, the similar pathogenic strategies for <it>C. neoformans </it>in murine and human cells supports the hypothesis that the mechanism that underlies the mammalian intracellular pathogenesis of <it>C. neoformans </it>originated from interactions with a third host, possibly soil amoeboid predators, before the mammalian radiation.</p>
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