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    Laser-mediated rupture of chlamydial inclusions triggers pathogen egress and host cell necrosis

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    Author
    Kerr, MC; Gomez, GA; Ferguson, C; Tanzer, MC; Murphy, JM; Yap, AS; Parton, RG; Huston, WM; Teasdale, RD
    Date
    2017-03-10
    Source Title
    Nature Communications
    Publisher
    NATURE PUBLISHING GROUP
    University of Melbourne Author/s
    Murphy, James
    Affiliation
    Medical Biology (W.E.H.I.)
    Metadata
    Show full item record
    Document Type
    Journal Article
    Citations
    Kerr, M. C., Gomez, G. A., Ferguson, C., Tanzer, M. C., Murphy, J. M., Yap, A. S., Parton, R. G., Huston, W. M. & Teasdale, R. D. (2017). Laser-mediated rupture of chlamydial inclusions triggers pathogen egress and host cell necrosis. NATURE COMMUNICATIONS, 8 (1), https://doi.org/10.1038/ncomms14729.
    Access Status
    Open Access
    URI
    http://hdl.handle.net/11343/258308
    DOI
    10.1038/ncomms14729
    Abstract
    Remarkably little is known about how intracellular pathogens exit the host cell in order to infect new hosts. Pathogenic chlamydiae egress by first rupturing their replicative niche (the inclusion) before rapidly lysing the host cell. Here we apply a laser ablation strategy to specifically disrupt the chlamydial inclusion, thereby uncoupling inclusion rupture from the subsequent cell lysis and allowing us to dissect the molecular events involved in each step. Pharmacological inhibition of host cell calpains inhibits inclusion rupture, but not subsequent cell lysis. Further, we demonstrate that inclusion rupture triggers a rapid necrotic cell death pathway independent of BAK, BAX, RIP1 and caspases. Both processes work sequentially to efficiently liberate the pathogen from the host cytoplasm, promoting secondary infection. These results reconcile the pathogen's known capacity to promote host cell survival and induce cell death.

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