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Infection and Immunity, July 2002, p. 3793-3803, Vol. 70, No. 7
0019-9567/02/$04.00+0     DOI: 10.1128/IAI.70.7.3793-3803.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

Chlamydia trachomatis Induces Remodeling of the Actin Cytoskeleton during Attachment and Entry into HeLa Cells

Reynaldo A. Carabeo,1 Scott S. Grieshaber,1 Elizabeth Fischer,2 and Ted Hackstadt1*

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

Received 17 January 2002/ Returned for modification 4 March 2002/ Accepted 8 April 2002

To elucidate the host cell machinery utilized by Chlamydia trachomatis to invade epithelial cells, we examined the role of the actin cytoskeleton in the internalization of chlamydial elementary bodies (EBs). Treatment of HeLa cells with cytochalasin D markedly inhibited the internalization of C. trachomatis serovar L2 and D EBs. Association of EBs with HeLa cells induced localized actin polymerization at the site of attachment, as visualized by either phalloidin staining of fixed cells or the active recruitment of GFP-actin in viable infected cells. The recruitment of actin to the specific site of attachment was accompanied by dramatic changes in the morphology of cell surface microvilli. Ultrastructural studies revealed a transient microvillar hypertrophy that was dependent upon C. trachomatis attachment, mediated by structural components on the EBs, and cytochalasin D sensitive. In addition, a mutant CHO cell line that does not support entry of C. trachomatis serovar L2 did not display such microvillar hypertrophy following exposure to L2 EBs, which is in contrast to infection with serovar D, to which it is susceptible. We propose that C. trachomatis entry is facilitated by an active actin remodeling process that is induced by the attachment of this pathogen, resulting in distinct microvillar reorganization throughout the cell surface and the formation of a pedestal-like structure at the immediate site of attachment and entry.

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

Editor: B. B. Finlay

Infection and Immunity, July 2002, p. 3793-3803, Vol. 70, No. 7
0019-9567/02/$04.00+0     DOI: 10.1128/IAI.70.7.3793-3803.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.



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