Mitochondrion-dependent apoptosis is essential for rickettsia parkeri infection and replication in vector cells

Xin Ru Wang, Nicole Y. Burkhardt, Timothy J Kurtti, Jonathan D. Oliver, Lisa D. Price, Benjamin Cull, Cody J. Thorpe, Michalina Silva Thiel, Ulrike G Munderloh

Research output: Contribution to journalArticlepeer-review

Abstract

Apoptosis is an innate immune response induced by infection in eukaryotes that contributes significantly to protection from pathogens. However, little is known about the role of apoptosis in the interactions of arthropod vectors with the rickettsiae that they transmit. Rickettsia spp. are vector-borne obligately intracellular bacteria and display different degrees of virulence in their eukaryotic hosts. In this study, we found that infection with Rickettsia parkeri (Rp) activated the apoptosis pathway in an Amblyomma americanum tick cell line (AAE2), as evidenced by the loss of phospholipid membrane asymmetry and DNA fragmentations. Additionally, infection with Rp also led to apoptosis activation in cell lines of different tick species. Interestingly, suppressing apoptosis decreased Rp infection and replication, while the activation of apoptosis increased Rp accumulation at the early stage of infection. Moreover, mitochondrion-dependent apoptosis was essential for Rp infection and replication in vector cells, and apoptosis induction required intracellular rickettsia replication. We further showed that Rp utilizes two different survival strategies to modulate apoptosis in the arthropod vectors and mammalian host cells. There was no direct correlation between apoptosis activation in vector cells and rickettsial pathogenicity. These novel findings indicate a possible mechanism whereby apoptosis facilitates infection and replication of a Rickettsia sp. in an arthropod vector. These results contribute to our understanding of how the vector's responses to pathogen infection affect pathogen replication and therefore transmission.

Original languageEnglish (US)
Article numbere01209-20
JournalmSystems
Volume6
Issue number2
DOIs
StatePublished - Mar 2021

Bibliographical note

Funding Information:
We thank Guillermo Marqués from the University image centers at the University of Minnesota, Twin Cities, for insightful suggestion for improvement of the images. The study was financially supported by a grant to U.G.M. from the NIH (2R01AI049424) and a grant to U.G.M. from the Minnesota Agricultural Experiment Station (MIN-17-078). We declare no conflict of interest.

Publisher Copyright:
© 2021 Wang et al.

Keywords

  • Apoptosis
  • Mitochondria
  • Rickettsia
  • Rickettsia pathogenesis
  • Tick
  • Tickborne pathogens

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