Schizophrenia Bulletin Advance Access originally published online on February 23, 2007
Schizophrenia Bulletin 2007 33(3):745-751; doi:10.1093/schbul/sbm008
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Effects of Toxoplasma gondii Infection on the Brain
2 Department of Microbiology and Immunology, University of Michigan School of Medicine, Ann Arbor, MI 48109
3 Center for Molecular Medicine and Infectious Diseases, Department of Biomedical Sciences and Pathobiology, Virginia-Maryland Regional College of Veterinary Medicine, Virginia Polytechnic Institute and State University, Blacksburg, VA 24061
1 To whom correspondence should be addressed; tel: 540-231-2095, fax: 540-231-3426, e-mail: ysuzuki{at}vt.edu.
Toxoplasma gondii, an intracellular protozoan parasite, can infect humans in 3 different ways: ingestion of tissue cysts, ingestion of oocysts, or congenital infection with tachyzoites. After proliferation of tachyzoites in various organs during the acute stage, the parasite forms cysts preferentially in the brain and establishes a chronic infection, which is a balance between host immunity and the parasite's evasion of the immune response. A variety of brain cells, including astrocytes and neurons, can be infected. In vitro studies using non-brain cells have demonstrated profound effects of the infection on gene expression of host cells, including molecules that promote the immune response and those involved in signal transduction pathways, suggesting that similar effects could occur in infected brain cells. Interferon-
is the essential mediator of the immune response to control T. gondii in the brain and to maintain the latency of chronic infection. Infection also induces the production of a variety of cytokines by microglia, astrocytes, and neurons, which promote or suppress inflammatory responses. The strain (genotype) of T. gondii, genetic factors of the host, and probably the route of infection and the stage (tachyzoite, cyst, or oocyst) of the parasite initiating infection all contribute to the establishment of a balance between the host and the parasite and affect the outcome of the infection.
Keywords: toxoplasmosis / toxoplasmic encephalitis / cyst / cell-mediated immunity / genotype / major histocompatibility complex
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