Pathogenic microbes have evolved diverse strategies to invade the host, avoid the innate immune response and multiply. The invasion of human cells by pathogens is observed in food-borne illnesses caused by Salmonella, Shigella and Listeria as well as periodontal (gum) infections. Microbial invasion of host cells is largely achieved by the pathogens' usurping of host signaling pathways. A common target of pathogens is the host cell's actin cytoskeleton, which the microbes use for attachment, entry into cells, movement within and between cells and avoidance of phagocytosis.
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Figure 1. Confocal micrograph illustrating Salmonella (green, arrows) attaching to the actin cytoskeleton (red staining) and entering cultured mouse embryonic fibroblasts (MEFs). Bacteria gain entry into the cells after < 1 minute of exposure. |
The actin-binding protein IQGAP1 is an established regulator of normal cytoskeletal function and may play a role in the invasion of human cells by microbial pathogens. My laboratory is presently investigating the IQGAP1-mediated mechanisms by which Salmonella subverts the actin cytoskeleton to establish infection.
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Figure 2. Confocal micrographs illustrating the co-localization of actin (blue, far-left panel) with the actin-binding protein IQGAP1 (green, left panel). Notably, IQGAP1 is recruited to the sites of Salmonella invasion into HeLa cells (red, right panel).The co-localization of actin, IQGAP1 and Salmonella is illustrated in the merge (far-right panel). |
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Figure 3. Schematic diagram illustrates the hijacking of the host cell's actin cytoskeleton by Salmonella, allowing microbial invasion. This process may be regulated by IQGAP1. |