Vesicular interactions of the Chlamydia trachomatis inclusion are determined by chlamydial early protein synthesis rather than route of entry

Infect Immun. 1996 Dec;64(12):5366-72. doi: 10.1128/iai.64.12.5366-5372.1996.


Chlamydiae replicate intracellularly within a vacuole that has recently been characterized as intersecting an exocytic pathway. One of the initial events during chlamydial infection is the expression of a chlamydial early gene product(s) that effectively isolates the inclusion from the endocytic-lysosomal pathway and makes it fusogenic with sphingomyelin-containing exocytic vesicles. Associated with this change in vesicular interaction is the delivery of the vacuole to the peri-Golgi region of the host cell. Inhibition of chlamydial early transcription or translation causes Chlamydia trachomatis-containing vesicles to remain dispersed throughout the cytoplasm, where they eventually fuse with lysosomes. Chlamydiae that have been internalized by Fc-mediated endocytosis also avoid lysosomal digestion by a mechanism that requires chlamydial protein synthesis. These results suggest that the vesicular interactions of the chlamydial inclusion are defined by parasite-directed modification of the endocytic vesicle rather than by the route of internalization.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Bacterial Proteins / biosynthesis*
  • Chlamydia Infections / microbiology*
  • Chlamydia trachomatis / growth & development
  • Chlamydia trachomatis / physiology*
  • Chlamydia trachomatis / ultrastructure
  • HeLa Cells
  • Humans
  • Microscopy, Electron


  • Bacterial Proteins