| Title | Vesicular interactions of the Chlamydia trachomatis inclusion are determined by chlamydial early protein synthesis rather than route of entry. |
| Publication Type | Journal Article |
| Year of Publication | 1996 |
| Authors | Scidmore, MA, Rockey, DD, Fischer, ER, Heinzen, RA, Hackstadt, T |
| Journal | Infect Immun |
| Volume | 64 |
| Issue | 12 |
| Pagination | 5366-72 |
| Date Published | 1996 Dec |
| ISSN | 0019-9567 |
| Keywords | Bacterial Proteins, Chlamydia Infections, Chlamydia trachomatis, HeLa Cells, Humans, Microscopy, Electron |
| Abstract |
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.
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| DOI | 10.1128/IAI.64.12.5366-5372.1996 |
| Alternate Journal | Infect Immun |
| PubMed ID | 8945589 |
| PubMed Central ID | PMC174531 |
| Grant List | N01-HD-2-3144 / HD / NICHD NIH HHS / United States |