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Infection and Immunity, February 2001, p. 1109-1119, Vol. 69, No. 2
Division of Infectious Diseases, School of
Public Health, University of California, Berkeley, California
94720,1 and The Francis I. Proctor
Foundation, University of California, San Francisco, California
941432
Received 5 July 2000/Returned for modification 16 August
2000/Accepted 25 October 2000
Chlamydia organisms are obligate intracellular
bacterial pathogens responsible for a range of human diseases.
Persistent infection or reinfection with Chlamydia
trachomatis leads to scarring of ocular or genital tissues, and
Chlamydia pneumoniae infection is associated with the
development of atherosclerosis. We demonstrate that C. trachomatis and C. pneumoniae infection in vitro
elicits the externalization of the lipid phosphatidylserine on the
surface of human epithelial, endothelial, granulocytic, and monocytic cells. Phosphatidylserine externalization is associated with cellular development, differentiation, and death. Infection-induced
phosphatidylserine externalization was immediate, transient, calcium
dependent, and infectious dose dependent and was unaffected by a
broad-spectrum caspase inhibitor. Chlamydia-infected cells
accelerated plasma clotting and increased the macrophage phagocytosis
of infected cells that was phosphatidylserine dependent. The rapid
externalization of phosphatidylserine by infected cells may be an
important factor in the pathogenesis of chlamydial infections.
0019-9567/01/$04.00+0 DOI: 10.1128/IAI.69.2.1109-1119.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.
Rapid, Transient Phosphatidylserine Externalization
Induced in Host Cells by Infection with Chlamydia spp.
*
Corresponding author. Mailing address: 235 Warren Hall,
Division of Infectious Diseases, School of Public Health, University of
California, Berkeley, CA 94720-7360. Phone: (510) 643-9900. Fax: (510)
643-1537. E-mail: rss{at}uclink4.berkeley.edu.
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