Infect Immun. 2006 Nov 6; [Epub ahead of print]
Infection with Toxoplasma bradyzoites has a diminished impact on host transcript levels relative to tachyzoite-infection.
Fouts AE, Boothroyd JC.
Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, CA 94305-5124, USA.
Toxoplasma gondii, an intracellular pathogen, has the potential to infect nearly every warm-blooded animal but rarely causes morbidity. The ability for the parasite to convert to the bradyzoite stage and live inside slow growing cysts that can go unnoticed by the host immune system allows for parasite persistence for the life of the infected host. This intracellular survival likely necessitates host cell modulation and tachyzoites are known to modify a number of signaling cascades within the host to promote parasite survival. Little is known, however, about how bradyzoites manipulate their host cell. Microarrays were used to profile the host transcriptional changes caused by bradyzoite-infection and compared with those of tachyzoite-infected and uninfected host cells 2 days post-infection in vitro. Infection resulted in chemokine, cytokine, extracellular matrix, and growth factor transcript level changes. A small group of genes were specifically induced by tachyzoite-infection, including CSF2, BCL2A1 and IL24, whereas bradyzoite-infection yielded only about half the changes seen with tachyzoite-infection and those changes that did occur were almost all of lower magnitude than those induced by tachyzoites. These results suggest that bradyzoites lead a more stealthy existence within the infected host cell.