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Infection and Immunity, February 2001, p. 968-976, Vol. 69, No. 2
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.2.968-976.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Infectivity of Chlamydia trachomatis Serovar LGV but Not E Is Dependent on Host Cell Heparan Sulfate

Maria Taraktchoglou,1 Allan A. Pacey,2 Jeremy E. Turnbull,3 and Adrian Eley1,*

Division of Genomic Medicine, The Medical School, The University of Sheffield, Sheffield, S10 2RX,1 University Department of Obstetrics and Gynecology, Jessop Hospital for Women, Sheffield, S3 7RE,2 and Molecular Cell Biology Research Laboratories, School of Biosciences, University of Birmingham, Edgbaston, Birmingham, B15 2TT,3 United Kingdom

Received 30 June 2000/Returned for modification 31 August 2000/Accepted 13 November 2000

The ability of heparan sulfate, heparin, and other glycosaminoglycans to inhibit the infectivity of Chlamydia trachomatis serovars E and LGV was examined using a simple competitive inhibition assay with three cell types from the human female reproductive tract, including primary human endosalpingeal cells. With the majority of the glycosaminoglycans tested, LGV was more significantly inhibited than serovar E. We have compared chlamydial infectivity between a wild-type Chinese hamster ovary cell line and two glycosaminoglycan-deficient cell lines. LGV was shown to be unable to infect heparan sulfate-deficient and GAG-deficient Chinese hamster ovary cell lines, whereas the E serovar infected these cells as efficiently as the control (nondeficient) cells. These two sets of experiments confirmed that serovar LGV is more dependent on a heparan sulfate-related mechanism of infectivity than is serovar E. This is further supported by the fact that attempts to purify a heparan sulfate-like molecule from either serovar cultured in glycosaminoglycan-deficient cell lines were nonproductive. Previous reports have suggested that chlamydia are able to produce a heparan sulfate-like molecule that is important for attachment and infectivity. We have attempted to detect possible binding of a specific heparan sulfate antibody to C. trachomatis by flow cytometry. Results showed no binding of the heparan sulfate antibody to C. trachomatis serovar LGV or E. Our results strongly indicate that chlamydiae do not produce a heparan sulfate-like molecule but rather use host cell heparan sulfate in order to infect cells.

* Corresponding author. Mailing address: Division of Genomic Medicine, The Medical School, The University of Sheffield, Beech Hill Rd., Sheffield, S10 2RX, United Kingdom. Phone: 44 (0) 114 272 4072. Fax: 44 (0) 114 273 9926. E-mail: a.r.eley{at}sheffield.ac.uk.

Infection and Immunity, February 2001, p. 968-976, Vol. 69, No. 2
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.2.968-976.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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