English
 
Help Privacy Policy Disclaimer
  Advanced SearchBrowse

Item

ITEM ACTIONSEXPORT

Released

Journal Article

Parasite-induced ER stress response in hepatocytes facilitates Plasmodium liver stage infection

MPS-Authors
/persons/resource/persons78437

Nagaraj,  Nagarjuna
Mann, Matthias / Proteomics and Signal Transduction, Max Planck Institute of Biochemistry, Max Planck Society;

/persons/resource/persons78356

Mann,  Matthias
Mann, Matthias / Proteomics and Signal Transduction, Max Planck Institute of Biochemistry, Max Planck Society;

External Resource
No external resources are shared
Fulltext (restricted access)
There are currently no full texts shared for your IP range.
Fulltext (public)
Supplementary Material (public)
There is no public supplementary material available
Citation

Inacio, P., Zuzarte-Luis, V., Ruivo, M. T. G., Falkard, B., Nagaraj, N., Rooijers, K., et al. (2015). Parasite-induced ER stress response in hepatocytes facilitates Plasmodium liver stage infection. EMBO REPORTS, 16(8), 955-964. doi:10.15252/embr.201439979.


Cite as: https://hdl.handle.net/11858/00-001M-0000-0028-45A5-3
Abstract
Upon infection of a mammalian host, Plasmodium parasites first replicate inside hepatocytes, generating thousands of new parasites. Although Plasmodium intra-hepatic development represents a substantial metabolic challenge to the host hepatocyte, how infected cells respond to and integrate this stress remains poorly understood. Here, we present proteomic and transcriptomic analyses, revealing that the endoplasmic reticulum (ER)-resident unfolded protein response (UPR) is activated in host hepatocytes upon Plasmodium berghei infection. The expression of XBP1s-the active form of the UPR mediator XBP1-and the liver-specific UPR mediator CREBH is induced by P. berghei infection in vivo. Furthermore, this UPR induction increases parasite liver burden. Altogether, our data suggest that ER stress is a central feature of P. berghei intra-hepatic development, contributing to the success of infection.