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Infection and Immunity, August 2005, p. 4620-4625, Vol. 73, No. 8
0019-9567/05/$08.00+0     doi:10.1128/IAI.73.8.4620-4625.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Chlamydia pneumoniae Uses the Mannose 6-Phosphate/Insulin-Like Growth Factor 2 Receptor for Infection of Endothelial Cells

Mirja Puolakkainen,{dagger} Cho-Chou Kuo, and Lee Ann Campbell*

Department of Pathobiology, University of Washington, Seattle, Washington

Received 8 February 2005/ Accepted 13 April 2005

Several mechanisms for attachment and entry of Chlamydia have been proposed. We previously determined that the major outer membrane protein of Chlamydia trachomatis is glycosylated with a high-mannose oligosaccharide, and a similar structure inhibited the attachment and infectivity of C. trachomatis in epithelial cells. Because insulin-like growth factor 2 (IGF2) was shown to enhance the infectivity of Chlamydia pneumoniae but not C. trachomatis in endothelial cells, a hapten inhibition assay was used to analyze whether the mannose 6-phosphate (M6P)/IGF2 receptor that also binds M6P could be involved in infection of endothelial cells (HMEC-1) by Chlamydia. M6P and mannose 6-phosphate-poly[N-(2-hydroxyethyl)-acrylamide] (M6P-PAA) inhibited the infectivity of C. pneumoniae AR-39, but not C. trachomatis serovar UW5 or L2, while mannan inhibited the growth of C. trachomatis, but not C. pneumoniae. Using metabolically labeled organisms incubated with cells at 4°C (organisms attach but do not enter) or at 37°C (organisms attach and are internalized), M6P-PAA was shown to inhibit attachment and internalization of C. pneumoniae in endothelial cells but did not inhibit attachment or internalization of C. trachomatis serovar E or L2. These findings indicate that C. pneumoniae can utilize the M6P/IGF2 receptor and that the use of this receptor for attachment and entry differs between C. pneumoniae and C. trachomatis.

* Corresponding author. Mailing address: Department of Pathobiology, Box 357238, University of Washington, Seattle, WA 98195. Phone: (206) 543-8689. Fax: (206) 543-3873. E-mail: lacamp{at}washington.edu.

Editor: J. T. Barbieri

{dagger} Present address: Haartman Institute, Department of Virology, PO Box 21, FIN-00014 University of Helsinki, Helsinki, Finland.

Infection and Immunity, August 2005, p. 4620-4625, Vol. 73, No. 8
0019-9567/05/$08.00+0     doi:10.1128/IAI.73.8.4620-4625.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.





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