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Quantitative 3D Imaging of Trypanosoma cruzi-Infected Cells, Dormant Amastigotes, and T Cells in Intact Clarified Organs
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Trypanosoma cruzi targets Akt in host cells as an intracellular antiapoptotic strategy

Marina V Chuenkova1, Mercio PereiraPerrin

  • 1Parasitology Research Center, Department of Pathology, Tufts University School of Medicine, 150 Harrison Avenue, Boston, MA 02111, USA.

Science Signaling
|November 19, 2009
PubMed

Insights

The parasite Trypanosoma cruzi uses parasite-derived neurotrophic factor (PDNF) to protect host cells from apoptosis. PDNF activates the antiapoptotic molecule Akt, promoting cell survival during Chagas' disease infection.

Area of Science:

  • Parasitology
  • Cell Biology
  • Molecular Biology

Background:

  • Trypanosoma cruzi causes Chagas' disease, requiring host cell survival for parasite replication.
  • Parasite differentiation and replication occur within the host cell cytosol.
  • Host cell survival is crucial for the progression of T. cruzi infection.

Purpose of the Study:

  • To investigate the role of parasite-derived neurotrophic factor (PDNF) in host cell survival.
  • To elucidate the molecular mechanisms by which PDNF protects host cells from apoptosis.
  • To understand how T. cruzi manipulates host cell machinery for its own benefit.

Main Methods:

  • Biochemical assays to determine PDNF's interaction with Akt.
  • Gene expression analysis to assess the impact of PDNF on apoptotic and antiapoptotic factors.
  • Cell-based assays to evaluate host cell protection against apoptosis induced by various stressors.

Main Results:

  • PDNF, a trans-sialidase on T. cruzi surface, acts as both a substrate and activator of the antiapoptotic kinase Akt.
  • PDNF upregulates Akt gene expression and downregulates proapoptotic gene transcription.
  • PDNF confers sustained protection to host cells against oxidative stress and inflammatory cytokines (TNF-α, TGF-β).

Conclusions:

  • PDNF is a key factor in T. cruzi's strategy to ensure host cell longevity.
  • PDNF activates Akt-mediated antiapoptotic signaling, both intracellularly and potentially via cell surface receptor TrkA.
  • This dual action of PDNF highlights a sophisticated mechanism employed by T. cruzi to promote infection persistence.

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