Cell invasion by un-palatable parasites.
While some intracellular pathogens invade and replicate exclusively in phagocytic host cells, others have evolved mechanisms to stimulate their uptake by cells not equipped with a well-developed phagocytic machinery. A common mechanism utilized by bacteria involves the induction of macropinocytosis, or of other F-actin-driven processes which result in engulfment of the pathogen through formation of a plasma membrane-derived vacuole. Interestingly, this type of "induced phagocytosis" mechanism does not appear to be utilized by protozoan parasites, which are significantly larger than bacteria in size (about 5-10 microns in average length). Intracellular protozoa either restrict themselves to infecting "professional" phagocytes (one example is the trypanosomatid Leishmania), or utilize highly unusual mechanisms for gaining access to the intracellular environment. Here we discuss what has been revealed in recent years about the remarkable cell invasion strategies of two highly successful intracellular parasites: Toxoplasma gondii and Trypanosoma cruzi. Toxoplasma utilizes a distinct form of actin/myosin-dependent gliding motility to propel itself into mammalian cells, while T. cruzi invades by subverting a Ca(2+)-regulated lysosomal exocytic pathway.
Sibley
L D
LD
Department of Molecular Microbiology, Washington University School of Medicine, 660 S. Euclid Avenue, St Louis, MO 63110, USA.
Andrews
N W
NW
D000199:Actins / Q000378:metabolism; D000818:Animals; D002462:Cell Membrane / Q000378:metabolism; D007891:Leishmania / Q000472:pathogenicity; D008247:Lysosomes / Q000378:metabolism; D008954:Models, Biological; D010271:Parasites / Q000378:metabolism* / Q000472:pathogenicity*; D010587:Phagocytosis; D010873:Pinocytosis; D015398:Signal Transduction; D014122:Toxoplasma / Q000472:pathogenicity; D014349:Trypanosoma cruzi / Q000472:pathogenicity
D000199:Actins