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Lec 8: Determinants of Infectious Disease 1 (AB)

Terms in this set (17)

=Some pathogens penetrate cells and survive intracelularly
-Few are obligate intracellular (Rickettsia spp., Mycobacterium leprae.)
-Others use as means of proliferation or spreading
-Phagocytic cells invaded through phagocytosis
-Non-phagocytic cells invaded using systems that induce a phagocytosis-like process.

-->Surviving phagocytosis:
-Reside in the phagolysosome (Coxiella burnetti)
-Reside in unfused phagosome (Mycobacterium spp., Salmonella spp.)
-Destroy/escape from phagosome + live in cytosol (Lysteria monocytogenes, Rickettsia rickettsii)
^i.e. immune system failed to eradicate
---------------------------------
-->Invading non-phagocytic cells
-Bacterial proteins recruit host proteins to induce phagocytosis
-E.g. secretion system used by gram neg bacteria (salmonella, pseudomonas)
-Invasion proteins injected
-Activate host signalling and recruit actin

^Confusing so here's the explanation from the internet:

-Some bacteria invade cells that are normally nonphagocytic. One way that bacteria can induce such a cell to phagocytose them is by expressing an adhesin that binds with high affinity to a cell adhesion protein that the cell normally uses to adhere to another cell or to the extracellular matrix. Binding to these transmembrane adhesion proteins fools the host cell into attempting to form a cell junction, and it begins moving actin and other cytoskeletal components to the site of bacterial attachment. Since the bacterium is small relative to the host cell, the host cell's attempt to spread over the adhesive surface of the bacterium results in the phagocytic uptake of the bacterium—a process known as the zipper mechanism of invasion.

-A second pathway by which bacteria can invade nonphagocytic cells is known as the trigger mechanism. It is used by various pathogens, including Salmonella enterica, which causes food poisoning. This dramatic form of invasion is initiated when the bacterium injects a set of effector molecules into the host cell cytoplasm through a type III secretion system. Some of these effector molecules activate Rho-family GTPases, which stimulate actin polymerization (discussed in Chapter 16). Others interact with cytoskeletal elements more directly, severing actin filaments and causing the rearrangement of cross-linking proteins. The net effect is to cause dramatic localized ruffling on the surface of the host cell, which throws up large actin-rich protrusions that fold over and trap the bacterium within large endocytic vesicles called macropinosomes.