MELS223 Lecture Notes - Lecture 12: Toxoplasma Gondii, Response Surface Methodology, Macrophage
6 Sep 2013
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Document Summary
Three basic mechanisms: interaction with host surface receptors listeria, yersinia, injection of bacterial effectors into host cytosol- salmonella, Shigella: active penetration into the host cell toxoplasma, plasmodium. Roles of invasion: access to environment suitable for growth (inside cell, protection from host antibody response surface are more prone, transversal of anatomical barriers. Salmonella will stay in phagosome and modify it. Listeria monocytogenes exits phagosome and stays within cell cytosol even when internalizing into the next adjacent cell. Bacteria are protected from host antibody response 1 by 1. Intestinal liver via blood through blood-brain-barrier, fetal/placental barrier. Inl interacts with surface receptors on human cell call e-cadherin. Internalization of listeria is driven by highly localized changes in host f-actin cytoskeleton. Salmonella enterica, serovar typhi : allows transversal of anatomical barriers. Salmonella involves large scale re-modelling(ruffles) of host cell surface. Many bacteria move in at once through a ruffle. Small gtpases regulate the actin cytoskeleton in mammalian cells.
