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Infection and Immunity, March 2006, p. 1795-1799, Vol. 74, No. 3
0019-9567/06/$08.00+0     doi:10.1128/IAI.74.3.1795-1799.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Interaction of Chlamydia trachomatis with Mammalian Cells Is Independent of Host Cell Surface Heparan Sulfate Glycosaminoglycans

Richard S. Stephens,1,2* Jesse M. Poteralski,1,2 and Lynn Olinger2

Division of Infectious Diseases, School of Public Health, University of California, Berkeley, California 94720,1 Francis I. Proctor Foundation, University of California, San Francisco, California 941432

Received 18 August 2005/ Returned for modification 27 September 2005/ Accepted 5 December 2005

The hypothesis that host cell surface heparan sulfate is required to promote chlamydial infection was tested using a cell line (CHO-18.4) containing a single retroviral insertion and the concomitant loss of heparan sulfate biosynthesis. Tests of chlamydial infectivity of heparan sulfate-deficient CHO-18.4 cells and parental cells, CHO-22, demonstrated that both were equally sensitive to infection by Chlamydia trachomatis serovars L2 and D. These data do not support the hypothesis and demonstrate that host cell surface heparan sulfate does not serve an essential functional role in chlamydial infectivity.


* Corresponding author. Mailing address: Division of Infectious Diseases, School of Public Health, 140 Earl Warren Hall, University of California, Berkeley, CA 94720. Phone: (510) 643-9900. Fax: (510) 643-1537. E-mail: RSS{at}Berkeley.edu.

Editor: J. N. Weiser


Infection and Immunity, March 2006, p. 1795-1799, Vol. 74, No. 3
0019-9567/06/$08.00+0     doi:10.1128/IAI.74.3.1795-1799.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.




This article has been cited by other articles:

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