Intracellular survival by Chlamydia.
Chlamydiae are obligate intracellular bacterial pathogens whose entry into mucosal epithelial cells is required for intracellular survival and subsequent growth. After a seemingly stealthy entry, chlamydiae quickly modify their vacuole (i) for exit from the endosomal pathway to the exocytic pathway and (ii) to permit fusion with intercepted endoplasmic reticulum- and Golgi-derived vesicles carrying glycerophospholipids and sphingolipids for chlamydiae-containing vacuole membrane expansion. Chlamydiae possess novel hollow proteinaceous structures, termed projections, which they use to pierce the inclusion membrane, possibly to acquire from the epithelial cytoplasm nutrients they cannot synthesize; whether or not these truncated flagellar-like structures serve a dual exchange function for secretion of molecules to programme host cell signalling is unknown. Despite the accumulation of some 500-1000 progeny in the enormously enlarged inclusion, host cell function is surprisingly little disrupted, and progeny escape can be unobtrusive. This elegant adaptive pathogen strategy, which leads to silent, chronic human infection, is fascinating from a cellular microbiology perspective.
Wyrick
P B
PB
Department of Microbiology and Immunology, University of North Carolina School of Medicine, Chapel Hill 27599-7290, USA. pbwyrick@etsu.edu
D022081:Cell Surface Extensions / Q000648:ultrastructure; D002689:Chlamydia / Q000737:chemistry / Q000472:pathogenicity* / Q000648:ultrastructure; D004721:Endoplasmic Reticulum / Q000378:metabolism; D011992:Endosomes / Q000378:metabolism / Q000382:microbiology; D004847:Epithelial Cells / Q000382:microbiology*; D020404:Glycerophospholipids; D006056:Golgi Apparatus / Q000737:chemistry / Q000378:metabolism; D006801:Humans; D013107:Sphingolipids; D013997:Time Factors
D020404:Glycerophospholipids; D013107:Sphingolipids