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Article
Heparin-mediated inhibition of Chlamydia psittaci adherence to HeLa cells
Microbial Pathogenesis
  • Cesar Gutiérrez-Martín, Institut Pasteur
  • David M. Ojcius, Institut Pasteur
  • Ru-Ching Hsia, London School of Hygiene and Tropical Medicine
  • Raymond Hellio, Institut Pasteur
  • Patrik M. Bavoil, London School of Hygiene and Tropical Medicine
  • Alice Dautry-Varsat, Institut Pasteur
ORCiD
David M. Ojcius: 0000-0003-1461-4495
Document Type
Article
DOI
10.1006/mpat.1996.0090
Publication Date
1-1-1997
Abstract
The adherence of human strains ofChlamydia trachomatishas been recently shown to be inhibitable by heparin and heparitinase, leading to the proposal thatChlamydiabinding to host cells may be mediated by a glycosaminoglycan (GAG)-dependent mechanism. We here describe the adherence of the guinea-pig pathogen,Chlamydia psittaciGPIC, to HeLa cells, which was measured by cytofluorometry with chlamydiae whose DNA was fluorescently labelled. Adherence could be inhibited by heat or trypsin pretreatment of the bacteria, and binding was much faster at 37°C (reaching a plateau within 1 h) than 4°C. Little binding remained when host cells were pre-fixed with paraformaldehyde, suggesting that host cell receptor mobility may be required for effective adherence. Visualization by confocal microscopy confirmed that the bacteria were at or near the host cell surface during the entire time-course of these experiments. Adherence increased as a function of pH between pH 6 and pH 8.0–8.5. Both adherence and infection of HeLa cells could be inhibited with heparin when the adherence step was performed at 4°C, but only infection was inhibited when the adherence step was performed at 37°C, even though heparitinase could block adherence at either 4°C or 37°C. Even at 4°C, heparin-mediated inhibition was significantly lower at pH 8 than pH 7.4, suggesting that GAG-independent mechanisms may play a role in the higher adherence observed at basic pH. These results therefore demonstrate that a GAG-dependent adherence step may be operative inC. psittaci, and raise the possibility that other adherence mechanisms may also contribute to binding by this chlamydial strain. Furthermore, they suggest that there may not be a strict correlation betweenC. psittaciadherence and the ability to cause productive infections.
Citation Information
Cesar Gutiérrez-Martín, David M. Ojcius, Ru-Ching Hsia, Raymond Hellio, et al.. "Heparin-mediated inhibition of Chlamydia psittaci adherence to HeLa cells" Microbial Pathogenesis Vol. 22 Iss. 1 (1997) p. 47 - 57 ISSN: 0882-4010
Available at: http://works.bepress.com/david-ojcius/104/