Mechanisms underlying the manipulation of host apoptotic pathways by Toxoplasma gondii

A. P. Sinai, T. M. Payne, J. C. Carmen, L. Hardi, S. J. Watson, R. E. Molestina

Research output: Contribution to journalReview articlepeer-review

69 Scopus citations


The establishment of a productive infection by an obligate intracellular pathogen is dependent on subversion of cellular defences. Apoptosis, or programmed cell death, is a property of metazoan cells that plays a critical role in inhibiting the proliferation of invasive organisms and viruses thereby protecting uninfected cells and limiting damage to the host organism. Not surprisingly, manipulation of the machinery of apoptosis plays a critical role in the pathogenesis of several intracellular pathogens. Toxoplasma gondii, arguably one of the most successful protozoan pathogens, has evolved several strategies to inhibit both the initiation and propagation of the apoptotic cascade. Recent work from several groups indicates an exquisite level of sophistication in the mechanisms to inhibit apoptosis along its diverse pathways. Much of this ability appears to centre around the manipulation of host transcription, specifically of genes involved in the pro-survival/anti- apoptotic response effectively manipulating the infected cell into a highly anti-apoptotic state. The implications of these observations extend beyond Toxoplasma biology to the broader area of microbial pathogenesis and cell signalling in mammalian cells.

Original languageEnglish
Pages (from-to)381-391
Number of pages11
JournalInternational Journal for Parasitology
Issue number3
StatePublished - Mar 9 2004

Bibliographical note

Funding Information:
This work is dedicated by APS to the memory of Dr. Andreina Liendo Gallejo Ph.D. a Scientist, Colleague and friend. We thank Drs David Roos and John Boothroyd for sharing data prior to publication. The technical assistance of the staff of the University of Kentucky Medical Center Electron Microscopy and Imaging Suite is gratefully acknowledged. Work in the Sinai lab is supported by NIAID grant AI49367. In addition REM is a recipient of an NIH/NRSA postdoctoral grant 1F32AI056970 and JCC is supported by a departmental training grant NIAID T32 AI 49795.


  • Apoptosis
  • Bcl2
  • Mitochondria
  • NFκB
  • Toxoplasma gondii

ASJC Scopus subject areas

  • Parasitology
  • Infectious Diseases


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