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Infection and Immunity, February 2004, p. 678-683, Vol. 72, No. 2
0019-9567/04/$08.00+0 DOI: 10.1128/IAI.72.2.678-683.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.
Department of Medicine, Washington University School of Medicine, St. Louis, Missouri 63110,1 Department of Biological Chemistry, Weizmann Institute of Science, Rehovot 76100, Israel2
Received 24 September 2003/ Returned for modification 27 October 2003/ Accepted 1 November 2003
Entamoeba histolytica trophozoites produce amoebapores, a family of small amphipathic peptides capable of insertion into bacterial or eukaryotic membranes and causing cellular lysis. Recently, E. histolytica trophozoites that are totally deficient in the production of amoebapore-A were created through a gene silencing mechanism (R. Bracha, Y. Nuchamowitz, and D. Mirelman, Eukaryot. Cell 2:295-305, 2003). Here we tested the virulence of amoebapore A(-) trophozoites in models of the two major forms of amebic disease: amebic liver abscess and amebic colitis. We demonstrate that amoebapore expression is required for full virulence in the SCID mouse model of amebic liver abscess, but E. histolytica trophozoites that do not express amoebapore-A can still cause inflammation and tissue damage in infected human colonic xenografts. These data are consistent with the concept that tissue damage may proceed by different mechanisms in amebic liver abscess compared to amebic colitis.
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