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Anja Schmidt-Christensen

Assistant researcher

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The liver stage of Plasmodium berghei inhibits host cell apoptosis

Author

  • Claudia Van De Sand
  • Sebastian Horstmann
  • Anja Schmidt
  • Angelika Sturm
  • Stefanie Bolte
  • Andreas Krueger
  • Marc Lütgehetmann
  • Jörg Matthias Pollok
  • Claude Libert
  • Volker T. Heussler

Summary, in English

Plasmodium berghei is the causative agent of rodent malaria and is widely used as a model system to study the liver stage of Plasmodium parasites. The entry of P. berghei sporozoites into hepatocytes has extensively been studied, but little is known about parasite-host interaction during later developmental stages of the intracellular parasite. Growth of the parasite far beyond the normal size of the host cell is an important stress factor for the infected cell. Cell stress is known to trigger programmed cell death (apoptosis) and we examined several apoptotic markers in P. berghei-infected cells and compared their level of expression and their distribution to that of non-infected cells. As none of the apoptotic markers investigated were found altered in infected cells, we hypothesized that parasite infection might confer resistance to apoptosis of the host cell. Treatment with peroxide or serum deprivation induced apoptosis in non-infected HepG2 cells, whereas P. berghei-infected cells appeared protected, indicating that the parasite interferes indeed with the apoptotic machinery of the host cell. To prove the physiological relevance of these results, mice were infected with high numbers of P. berghei sporozoites and treated with tumour necrosis factor (TNF)-α/D-galactosamine to induce massive liver apoptosis. Liver sections of these mice, stained for degraded DNA, confirmed that infected cells containing viable parasites were protected from programmed cell death. However, in non-treated control mice as well as in TNF-α-treated mice a small proportion of dead intracellular parasites with degraded DNA were detected. Most hepatocytes containing dead parasites provoked an infiltration of immunocompetent cells, indicating that these cells are no longer protected from cell death.

Publishing year

2005-11

Language

English

Pages

731-742

Publication/Series

Molecular Microbiology

Volume

58

Issue

3

Document type

Journal article

Publisher

Wiley-Blackwell

Status

Published

ISBN/ISSN/Other

  • ISSN: 0950-382X