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Related Experiment Videos

Microarray analysis reveals previously unknown changes in Toxoplasma gondii-infected human cells.

I J Blader1, I D Manger, J C Boothroyd

  • 1Department of Microbiology and Immunology, Stanford University, Stanford, California 94305-5124, USA.

The Journal of Biological Chemistry
|April 11, 2001
PubMed
Summary

Toxoplasma gondii infection alters host cell gene expression, initially boosting immune responses via parasite secretions. Later, direct parasite presence modifies host cell processes like metabolism, revealing new host-pathogen interactions.

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Area of Science:

  • Cellular biology
  • Parasitology
  • Immunology

Background:

  • Toxoplasma gondii infection induces pro-inflammatory cytokines, organelle redistribution, and apoptosis resistance in host cells.
  • Understanding the molecular mechanisms behind these host cell alterations is crucial for studying host-pathogen interactions.

Purpose of the Study:

  • To investigate the gene expression profiles of human foreskin fibroblasts infected with Toxoplasma gondii.
  • To identify host genes modulated during early and late stages of infection.
  • To differentiate between host responses induced by parasite invasion versus secreted factors.

Main Methods:

  • Gene expression profiling using human cDNA microarrays (approx. 22,000 genes).
  • Infection of human foreskin fibroblasts with Toxoplasma gondii.

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  • Analysis of gene transcript abundance at early (1-2 h) and later time points post-infection.

    • Main Results:

    • Early infection (<1% of genes altered) showed up-regulation of immune response genes, triggered by parasite secretions alone.
    • Later infection revealed modulation of host cell processes, including glucose and mevalonate metabolism.
    • Late-stage gene modulation required direct parasite presence, not just secreted factors.

    Conclusions:

    • Toxoplasma gondii infection elicits distinct early and late host gene expression responses.
    • Early immune gene activation is mediated by secreted parasite factors, independent of invasion.
    • Later metabolic changes are dependent on the parasite's direct interaction with the host cell, highlighting novel host-pathogen interplay.