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Infect Immun. 2017 Apr 21;85(5). pii: e00046-17. doi: 10.1128/IAI.00046-17. Print 2017 May.

Chlamydia trachomatis Cellular Exit Alters Interactions with Host Dendritic Cells.

Author information

1
Division of Allergy and Infectious Diseases, Department of Medicine, University of Washington, Seattle, Washington, USA.
2
Division of Allergy and Infectious Diseases, Department of Medicine, University of Washington, Seattle, Washington, USA khybiske@uw.edu.

Abstract

The strategies utilized by pathogens to exit host cells are an area of pathogenesis which has received surprisingly little attention, considering the necessity of this step for infections to propagate. Even less is known about how exit through these pathways affects downstream host-pathogen interactions and the generation of an immune response. Chlamydia trachomatis exits host epithelial cells through two equally active mechanisms: lysis and extrusion. Studies have characterized the outcome of interactions between host innate immune cells, such as dendritic cells and macrophages, and free, extracellular Chlamydia bacteria, such as those resulting from lysis. Exit via extrusion generates a distinct, host-membrane-bound compartment of Chlamydia separate from the original infected cell. In this study, we assessed the effect of containment within extrusions upon the interaction between Chlamydia and host dendritic cells. Extrusion dramatically affected the outcome of Chlamydia-dendritic cell interactions for both the bacterium and the host cell. Dendritic cells rapidly underwent apoptosis in response to engulfment of an extrusion, while uptake of an equivalent dose of free Chlamydia had no such effect. Containment within an extrusion also prolonged bacterial survival within dendritic cells and altered the initial innate immune signaling by the dendritic cell.

KEYWORDS:

Chlamydia; apoptosis; dendritic cell; extrusion

PMID:
28223346
PMCID:
PMC5400845
DOI:
10.1128/IAI.00046-17
[Indexed for MEDLINE]
Free PMC Article

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