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Rapid, transient phosphatidylserine externalization induced in host cells by infection with Chlamydia spp
1Division of Infectious Diseases, School of Public Health, University of California, Berkeley, California 94720, USA.
Abstract:
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.
Insights
Chlamydia bacterial infections cause cells to expose phosphatidylserine, a lipid molecule. This externalization accelerates blood clotting and enhances macrophage engulfment of infected cells, impacting chlamydial disease.
Area of Science:
- Microbiology
- Cell Biology
- Immunology
Background:
- Chlamydia are obligate intracellular bacteria causing human diseases like ocular scarring and atherosclerosis.
- Understanding Chlamydia pathogenesis is crucial for developing effective treatments.
Purpose of the Study:
- To investigate the effect of Chlamydia trachomatis and Chlamydia pneumoniae infection on host cell membranes.
- To determine the role of phosphatidylserine externalization in Chlamydia pathogenesis.
Main Methods:
- In vitro infection of human epithelial, endothelial, granulocytic, and monocytic cells with Chlamydia.
- Analysis of phosphatidylserine externalization using flow cytometry and microscopy.
- Assays to measure plasma clotting time and macrophage phagocytosis.
Main Results:
- Chlamydia infection rapidly induced phosphatidylserine externalization in various human cell types.
- This process was calcium-dependent, transient, and infectious dose-dependent.
- Infected cells accelerated plasma clotting and enhanced macrophage phagocytosis in a phosphatidylserine-dependent manner.
- Caspase inhibition did not affect infection-induced phosphatidylserine externalization.
Conclusions:
- Chlamydia infection triggers phosphatidylserine externalization on host cells.
- This lipid exposure plays a significant role in Chlamydia pathogenesis by influencing coagulation and immune cell interactions.
- Targeting phosphatidylserine externalization may offer novel therapeutic strategies against chlamydial infections.