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Infection and Immunity, February 2003, p. 973-984, Vol. 71, No. 2
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.2.973-984.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

Restricted Fusion of Chlamydia trachomatis Vesicles with Endocytic Compartments during the Initial Stages of Infection

Marci A. Scidmore,1,{dagger} Elizabeth R. Fischer,2 and Ted Hackstadt1*

Host-Parasite Interactions Section, Laboratory of Intracellular Parasites,1 Microscopy Branch, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, Hamilton, Montana 598402

Received 9 August 2002/ Returned for modification 10 October 2002/ Accepted 4 November 2002

The chlamydial inclusion occupies a unique niche within the eukaryotic cell that does not interact with endocytic compartments but instead is fusogenic with a subset of sphingomyelin-containing exocytic vesicles. The Chlamydia trachomatis inclusion acquires these distinctive properties by as early as 2 h postinfection as demonstrated by the ability to acquire sphingomyelin, endogenously synthesized from 6{N-[(7-nitrobenzo-2-oxa-1,3-diazol-4-yl)amino]caproylsphingosine} (C6-NBD-ceramide). The molecular mechanisms involved in transformation of the properties and cellular interactions of the inclusion are unknown except that they require early chlamydial transcription and translation. Although the properties of the inclusion are established by 2 h postinfection, the degree of interaction with endocytic pathways during the brief interval before fusogenicity with an exocytic pathway is established is unknown. Using a combination of confocal and electron microscopy to localize endocytic and lysosomal markers in C. trachomatis infected cells during the early stages of infection, we demonstrate a lack of these markers within the inclusion membrane or lumen of the inclusion to conclude that the nascent chlamydial inclusion is minimally interactive with endosomal compartments during this interval early in infection. Even when prevented from modifying the properties of the inclusion by incubation in the presence of protein synthesis inhibitors, vesicles containing elementary bodies are very slow to acquire lysosomal characteristics. These results imply a two-stage mechanism for chlamydial avoidance of lysosomal fusion: (i) an initial phase of delayed maturation to lysosomes due to an intrinsic property of elementary bodies and (ii) an active modification of the vesicular interactions of the inclusion requiring chlamydial protein synthesis.

* Corresponding author. Mailing address: Host-Parasite Interactions Section, Laboratory of Intracellular Parasites, Rocky Mountain Laboratories, NIAID, Hamilton, MT 59840. Phone: (406) 363-9308. Fax: (406) 363-9253. E-mail: ted_hackstadt{at}nih.gov.

Editor: D. L. Burns

{dagger} Present address: Department of Microbiology and Immunology, Cornell University College of Veterinary Medicine, Ithaca, NY 14853.

Infection and Immunity, February 2003, p. 973-984, Vol. 71, No. 2
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.2.973-984.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.



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