ENTAMOEBA-HISTOLYTICA - TARGET-CELLS KILLED BY TROPHOZOITES UNDERGO DNA FRAGMENTATION WHICH IS NOT BLOCKED BY BCL-2

RAGLAND, BD; ASHLEY, LS; Vaux, DL; PETRI, WA

Author(s): RAGLAND, BD; ASHLEY, LS; Vaux, DL; PETRI, WA;
Details: Publication Year 1994-11,Volume 79,Issue #3,Page 460-467
Journal Title: EXPERIMENTAL PARASITOLOGY
Publication Type: Journal Article
Abstract: Amebic destruction of neutrophils and macrophages is contact-dependent. Adherence is mediated by a galactose-specific surface lectin on the amebic membrane. The pathway by which contact-dependent cytolysis of the target cell occurs is unknown. We hypothesized that target cell death is due to the triggering of apoptosis (programmed cell death) by the amebae. The purpose of this study was to determine whether target cell DNA is fragmented into a ladder pattern characteristic of apoptosis and to test whether overexpression of Bcl-2, a protein that confers resistance to apoptotic death from some stimuli, blocks target cell killing. The murine myeloid cell line FDC-P1 transfected with a retrovirus construct expressing the Bcl-2 protein was shown to be resistant to the apoptotic death that the parental line undergoes upon growth factor deprivation. Cr-51-labeled FDC-P1 control or bcl-2-transfected cells were incubated with Entamoeba histolytica (4:1 cell/ameba ratio) and killing of the cells was assessed by Cr-51 release. Both cell lines were susceptible to contact-dependent killing. Death induced by the amebae in the bcl-2-transfected cells resulted in a DNA ladder fragmentation pattern (using [I-125]iododeoxyuridine-labeled target cell DNA) identical to that seen in the control cells undergoing apoptosis upon growth factor withdrawal. Target cell DNA fragmentation was inhibited by blocking adherence with galactose. Our data suggest that target cell killing by E. histolytica can occur via Bcl-2-independent apoptotic mechanism. (C) 1994 Academic Press, Inc.
Publisher: ACADEMIC PRESS INC JNL-COMP SUBSCRIPTIONS
Keywords: DEATH GENE CED-3; PREVENT APOPTOSIS; PATHOGENICITY; MECHANISMS; EXPRESSION; CALCIUM; ENZYME
Publisher's Version: https://doi.org/10.1006/expr.1994.1107
Terms of Use/Rights Notice: Refer to copyright notice on published article.

Creation Date: 1994-11-01 12:00:00