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Mcl-1 Is a Key Regulator of Apoptosis Resistance in Chlamydia trachomatis-Infected Cells

MPG-Autoren
http://pubman.mpdl.mpg.de/cone/persons/resource/persons82110

Rajalingam,  Krishnaraj
Department of Molecular Biology, Max Planck Institute for Infection Biology, Max Planck Society;

http://pubman.mpdl.mpg.de/cone/persons/resource/persons82159

Sharma,  Manu
Department of Molecular Biology, Max Planck Institute for Infection Biology, Max Planck Society;

http://pubman.mpdl.mpg.de/cone/persons/resource/persons82022

Lohmann,  Christine
Department of Molecular Biology, Max Planck Institute for Infection Biology, Max Planck Society;

http://pubman.mpdl.mpg.de/cone/persons/resource/persons82081

Oswald,  Monique
Department of Molecular Biology, Max Planck Institute for Infection Biology, Max Planck Society;

http://pubman.mpdl.mpg.de/cone/persons/resource/persons82181

Thieck,  Oliver
Department of Molecular Biology, Max Planck Institute for Infection Biology, Max Planck Society;

http://pubman.mpdl.mpg.de/cone/persons/resource/persons82130

Rudel,  Thomas
Department of Molecular Biology, Max Planck Institute for Infection Biology, Max Planck Society;

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PLoS_One_2008_3_e3102.pdf
(Verlagsversion), 548KB

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Zitation

Rajalingam, K., Sharma, M., Lohmann, C., Oswald, M., Thieck, O., Froelich, C. J., et al. (2008). Mcl-1 Is a Key Regulator of Apoptosis Resistance in Chlamydia trachomatis-Infected Cells. PLoS ONE, 3(9): e3102. doi:10.1371/journal.pone.0003102.


Zitierlink: http://hdl.handle.net/11858/00-001M-0000-000E-C186-0
Zusammenfassung
Chlamydia are obligate intracellular bacteria that cause variety of human diseases. Host cells infected with Chlamydia are protected against many different apoptotic stimuli. The induction of apoptosis resistance is thought to be an important immune escape mechanism allowing Chlamydia to replicate inside the host cell. Infection with C. trachomatis activates the Raf/MEK/ERK pathway and the PI3K/AKT pathway. Here we show that inhibition of these two pathways by chemical inhibitors sensitized C. trachomatis infected cells to granzyme B-mediated cell death. Infection leads to the Raf/MEK/ERK-mediated up-regulation and PI3K-dependent stabilization of the anti-apoptotic Bcl-2 family member Mcl-1. Consistently, interfering with Mcl-1 up-regulation sensitized infected cells for apoptosis induced via the TNF receptor, DNA damage, granzyme B and stress. Our data suggest that Mcl-1 up-regulation is primarily required to maintain apoptosis resistance in C. trachomatis-infected cells.