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Chlamydia trachomatis fails to protect its growth niche against pro-apoptotic insults
Umeå universitet, Medicinska fakulteten, Institutionen för molekylärbiologi (Medicinska fakulteten). Umeå universitet, Medicinska fakulteten, Molekylär Infektionsmedicin, Sverige (MIMS). Umeå universitet, Medicinska fakulteten, Umeå Centre for Microbial Research (UCMR). INSERM U1138, Centre de Recherche des Cordeliers, Paris, France; Equipe 11 labellisée Ligue Nationale contre le Cancer, Centre de Recherche des Cordeliers, Paris, France; Université Paris Descartes, Paris, France; Metabolomics and Cell Biology Platforms, Institut Gustave Roussy, Villejuif, France. (Barbara Sixt)ORCID-id: 0000-0002-5607-8902
Umeå universitet, Medicinska fakulteten, Institutionen för klinisk mikrobiologi. Umeå universitet, Medicinska fakulteten, Molekylär Infektionsmedicin, Sverige (MIMS). Umeå universitet, Medicinska fakulteten, Umeå Centre for Microbial Research (UCMR). (Sven Bergström)
INSERM U1138, Centre de Recherche des Cordeliers; Equipe 11 labellisée Ligue Nationale contre le Cancer, Centre de Recherche des Cordeliers; Université Paris Descartes; Metabolomics and Cell Biology Platforms, Institut Gustave Roussy.
Duke University School of Medicine, Department of Molecular Genetics and Microbiology.
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2019 (Engelska)Ingår i: Cell Death and Differentiation, ISSN 1350-9047, E-ISSN 1476-5403, Vol. 26, nr 8, s. 1485-1500Artikel i tidskrift (Refereegranskat) Published
Abstract [en]

Chlamydia trachomatis is an obligate intracellular bacterial agent responsible for ocular infections and sexually transmitted diseases. It has been postulated that Chlamydia inhibits apoptosis in host cells to maintain an intact replicative niche until sufficient infectious progeny can be generated. Here we report that, while cells infected with C. trachomatis are protected from apoptosis at early and mid-stages of infection, they remain susceptible to the induction of other cell death modalities. By monitoring the fate of infected cells by time-lapse video microscopy and by analyzing host plasma membrane integrity and the activity of caspases, we determined that C. trachomatis-infected cells exposed to pro-apoptotic stimuli predominately died by a mechanism resembling necrosis. This necrotic death of infected cells occurred with kinetics similar to the induction of apoptosis in uninfected cells, indicating that C. trachomatis fails to considerably prolong the lifespan of its host cell when exposed to pro-apoptotic insults. Inhibitors of bacterial protein synthesis partially blocked necrotic death of infected cells, suggesting that the switch from apoptosis to necrosis relies on an active contribution of the bacteria. Tumor necrosis factor alpha (TNF-α)-mediated induction of necrosis in cells infected with C. trachomatis was not dependent on canonical regulators of necroptosis, such as RIPK1, RIPK3, or MLKL, yet was blocked by inhibition or depletion of CASP8. These results suggest that alternative signaling pathways regulate necrotic death in the context of C. trachomatis infections. Finally, consistent with the inability of C. trachomatis to preserve host cell viability, necrosis resulting from pro-apoptotic conditions significantly impaired production of infectious progeny. Taken together, our findings suggest that Chlamydia's anti-apoptotic activities are not sufficient to protect the pathogen's replicative niche.

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Nature Publishing Group, 2019. Vol. 26, nr 8, s. 1485-1500
Nationell ämneskategori
Mikrobiologi inom det medicinska området
Identifikatorer
URN: urn:nbn:se:umu:diva-153979DOI: 10.1038/s41418-018-0224-2ISI: 000480645800009PubMedID: 30375511OAI: oai:DiVA.org:umu-153979DiVA, id: diva2:1269648
Tillgänglig från: 2018-12-11 Skapad: 2018-12-11 Senast uppdaterad: 2019-08-30Bibliografiskt granskad

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Sixt, Barbara SusanneNúñez-Otero, Carlos

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Institutionen för molekylärbiologi (Medicinska fakulteten)Molekylär Infektionsmedicin, Sverige (MIMS)Umeå Centre for Microbial Research (UCMR)Institutionen för klinisk mikrobiologi
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