, Volume 41, Issue 4, pp 1372–1383 | Cite as

ERK1/2 and the Bcl-2 Family Proteins Mcl-1, tBid, and Bim Are Involved in Inhibition of Apoptosis During Persistent Chlamydia psittaci Infection

  • Li Li
  • Chuan Wang
  • Yating Wen
  • Yuming Hu
  • Yafeng Xie
  • Man Xu
  • Mingxing Liang
  • Wei Liu
  • Liangzhuan Liu
  • Yimou WuEmail author


Chlamydia psittaci is an obligate intracellular pathogen that can cause zoonosis. Persistent C. psittaci infection can inhibit apoptosis in host cells, thus extending their survival and enabling them to complete their growth cycle. In this study, the antiapoptotic effects of persistent C. psittaci infection, induced by treatment with IFN-γ, were found to be associated with both the death receptor and the mitochondrial pathways of apoptosis. These effects were mediated by Bcl-2 family members, as evidenced by the decreased expression of proapoptotic proteins, such as tBid and Bim. Simultaneously, the antiapoptotic protein Mcl-1 was upregulated by persistent C. psittaci infection. Increased phosphorylation of ERK1/2 was observed; however, the expression of Bad, unlike that of other proapoptotic proteins, did not seem to be involved in this process. In summary, persistent chlamydial infection exerts antiapoptotic effects through both the death receptor and the mitochondrial pathways, in a process that is regulated by the ERK1/2 and apoptotic proteins of the Bcl-2 family.


apoptosis Chlamydia psittaci persistent infection Bcl-2 family proteins IFN-γ 



Bcl-2 antagonist killer


Bcl-2 associated X


B-cell leukemia/lymphoma 2


BH3 interacting domain death agonist


Carbonyl cyanide 3-chlorophenylhydrazone

C. psittaci

Chlamydia psittaci


Elementary body


Fas-associated protein with death domain


Myeloid cell leukemia-1


Multiplicity of infection


Phosphate-buffered saline


Phosphorylation of ERK1/2


P53 upregulated modulator of apoptosis


Polyvinylidene difluoride


90-kDa ribosomal S6 kinase


Recombinant human gamma interferon


Sodium dodecyl sulfate





This work was supported by the National Natural Science Foundation of China (grant nos. 31270218 and 31300156), the Special Foundation of Hunan Provincial Science and Technology Department (grant no. 2013TT1003), and the Hunan Provincial Key Laboratory for Special Pathogens Prevention and Control Foundation (grant nos. 2014-5 and 2012-312).


Conflict of Interest

The authors declare that they have no conflict of interest.

Research Involving Human Participants and/or Animals

Not applicable.

Informed Consent

Not applicable.


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Copyright information

© Springer Science+Business Media, LLC, part of Springer Nature 2018

Authors and Affiliations

  • Li Li
    • 1
    • 2
  • Chuan Wang
    • 1
  • Yating Wen
    • 1
  • Yuming Hu
    • 2
  • Yafeng Xie
    • 1
  • Man Xu
    • 1
  • Mingxing Liang
    • 1
  • Wei Liu
    • 1
  • Liangzhuan Liu
    • 1
  • Yimou Wu
    • 1
    Email author
  1. 1.Hunan Provincial Key Laboratory for Special Pathogens Prevention and Control, Institute of Pathogenic Biology, Medical CollegeUniversity of South China, Hengyang, China; and Hunan Province Cooperative Innovation Center for Molecular Target New Drug StudyHengyangChina
  2. 2.Hunan Provincial Center for Disease Control and PreventionChangshaChina

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