Expression of amoebapores is required for full expression of Entamoeba histolytica virulence in amebic liver abscess but is not necessary for the induction of inflammation or tissue damage in amebic colitis.
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.
Zhang
Xiaochun
X
Department of Medicine, Washington University School of Medicine, St. Louis, Missouri 63110, USA.
Zhang
Zhi
Z
Alexander
Diane
D
Bracha
Rivka
R
Mirelman
David
D
Stanley
Samuel L
SL
D000818:Animals; D004404:Dysentery, Amebic / Q000209:etiology*; D004748:Entamoeba histolytica / Q000472:pathogenicity*; D007249:Inflammation / Q000209:etiology*; D007375:Interleukin-1 / Q000502:physiology; D016209:Interleukin-8 / Q000502:physiology; D007473:Ion Channels / Q000502:physiology*; D008101:Liver Abscess, Amebic / Q000209:etiology*; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D016513:Mice, SCID; D015800:Protozoan Proteins / Q000502:physiology*; D014774:Virulence
D007375:Interleukin-1; D016209:Interleukin-8; D007473:Ion Channels; D015800:Protozoan Proteins; C041670:amoebapore proteins, protozoan