Exploitation of host cells by Burkholderia pseudomallei.
Intracellular bacterial pathogens have evolved mechanisms to enter and exit eukaryotic cells using the power of actin polymerisation and to subvert the activity of cellular enzymes and signal transduction pathways. The proteins deployed by bacteria to subvert cellular processes often mimic eukaryotic proteins in their structure or function. Studies on the exploitation of host cells by the facultative intracellular pathogen Burkholderia pseudomallei are providing novel insights into the pathogenesis of melioidosis, a serious invasive disease of animals and humans that is endemic in tropical and subtropical areas. B. pseudomallei can invade epithelial cells, survive and proliferate inside phagocytes, escape from endocytic vesicles, form actin-based membrane protrusions and induce host cell fusion. Here we review current understanding of the molecular mechanisms underlying these processes.
Stevens
Mark P
MP
Division of Microbiology, Institute for Animal Health, Compton Laboratory, Berkshire, United Kingdom.
Galyov
Edouard E
EE
D000199:Actins / Q000276:immunology* / Q000502:physiology; D000818:Animals; D001425:Bacterial Outer Membrane Proteins / Q000276:immunology / Q000502:physiology; D016957:Burkholderia pseudomallei / Q000276:immunology / Q000472:pathogenicity / Q000502:physiology*; D003599:Cytoskeleton / Q000276:immunology* / Q000382:microbiology / Q000502:physiology; D006367:HeLa Cells; D006801:Humans; D008554:Melioidosis / Q000276:immunology / Q000382:microbiology* / Q000473:pathology; D010587:Phagocytosis / Q000276:immunology / Q000502:physiology; D022161:Transport Vesicles / Q000276:immunology / Q000382:microbiology / Q000502:physiology; D014774:Virulence
D000199:Actins; D001425:Bacterial Outer Membrane Proteins