The Journal of Experimental Medicine
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Published 17 June 2002. doi:10.1084/jem.20020258
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© Rockefeller University Press, 0022-1007/2002/6/1625/ $5.00
The Journal of Experimental Medicine, Volume 195, Number 12, June 17, 2002 1625-1633

Transepithelial Migration of Toxoplasma gondii Is Linked to Parasite Motility and Virulence

Antonio Barragan1,2 and L. David Sibley1

1 Department of Molecular Microbiology, Washington University School of Medicine, St. Louis, MO 63110
2 Center for Infectious Medicine, Karolinska Institutet, Department of Medicine, Huddinge University Hospital, SE-141 86 Stockholm, Sweden

Address correspondence to L. David Sibley, Department of Molecular Microbiology, Washington University School of Medicine, 660 S. Euclid Ave., St. Louis, MO 63110. Phone: 314-362-8873; Fax: 314-362-3203; E-mail: sibley{at}borcim.wustl.edu

After oral ingestion, Toxoplasma gondii crosses the intestinal epithelium, disseminates into the deep tissues, and traverses biological barriers such as the placenta and the blood-brain barrier to reach sites where it causes severe pathology. To examine the cellular basis of these processes, migration of T. gondii was studied in vitro using polarized host cell monolayers and extracellular matrix. Transmigration required active parasite motility and the highly virulent type I strains consistently exhibited a superior migratory capacity than the nonvirulent type II and type III strains. Type I strain parasites also demonstrated a greater capacity for transmigration across mouse intestine ex vivo, and directly penetrated into the lamina propria and vascular endothelium. A subpopulation of virulent type I parasites exhibited a long distance migration (LDM) phenotype in vitro, that was not expressed by nonvirulent type II and type III strains. Cloning of parasites expressing the LDM phenotype resulted in substantial increase of migratory capacity in vitro and in vivo. The potential to up-regulate migratory capacity in T. gondii likely plays an important role in establishing new infections and in dissemination upon reactivation of chronic infections.

Key Words: apicomplexa • dissemination • invasion • epithelium • barrier


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