By Richard J. Lamont
Knowing the molecular foundation of bacterial invasion and of host mobilephone version to intracellular micro organism will supply primary insights into the pathophysiology of micro organism and the mobile biology of the host. This publication information particular examples of micro organism which are masters of manipulation of eukaryotic telephone signaling and relates those occasions to the wider context of host-pathogen interplay. Written by way of specialists within the box, it will likely be of curiosity to researchers and graduate scholars in microbiology, immunology, and biochemistry, in addition to in molecular drugs and dentistry.
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Extra resources for Bacterial Invasion of Host Cells (Advances in Molecular and Cellular Microbiology)
The activation of Cdc42 and Rac1 triggers a series of signal transduction events that lead to actin cytoskeleton rearrangements. Despite their different biochemical activities, SopE/E2 and SopB exert at least partially redundant functions during Salmonella invasion. Thus, introduction of a loss-of-function mutation in the genes that encode either one of these proteins results in a minor defect in Salmonella entry. However, the simultaneous inactivation of SopE/E2 and SopB results in a very severe entry defect.
Typhimurium lacking the entirety of SPI-1 cannot invade tissue cells but nevertheless still disseminates to systemic organs in Balb/c mice following intragastric infection (Murray and Lee, 2001). This observation highlights a new important concept in Salmonella pathogenesis establishing that TTSS-1 may also have activities aside from inducing invasion-associated rearrangements inside nonphagocytic epithelial cells. It is now apparent that S. typhimurium attracts, kills, and parasitizes different immune cells, and some of these activities require TTSS-1.
An ipgD mutant still enters host cells; however, in comparison with that directed by the wild type, the morphology of the membrane ruffle is altered. , 2002). This finding, together with the increase in Shigella invasiveness in host cells treated with microtubule-destabilizing agents such as nocodazole, suggests that the bacteria have the ability to modulate tubulin dynamics. VirA has activity to trigger microtubule dynamic instability in vitro and in vivo, which can stimulate Rac1 activity, thus leading to membrane ruffling (Fig.