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Infect Immun, June 1998, p. 2980-2983, Vol. 66, No. 6
0019-9567/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.

Entamoeba histolytica Induces Host Cell Death in Amebic Liver Abscess by a Non-Fas-Dependent, Non-Tumor Necrosis Factor Alpha-Dependent Pathway of Apoptosis

Karl B. Seydel1,2 and Samuel L. Stanley Jr.1,2,*

Departments of Medicine1 and Molecular Microbiology,2 Washington University School of Medicine, St. Louis, Missouri 63110

Received 17 December 1997/Returned for modification 11 February 1998/Accepted 24 March 1998

Amebic liver abscess is characterized by extensive areas of dead hepatocytes that form cavities surrounded by a thin rim of inflammatory cells and few Entamoeba histolytica trophozoites. E. histolytica produces pore-forming proteins and proteinases, but how trophozoites actually kill host cells has been unclear. Here, we report that E. histolytica induces apoptosis in both inflammatory cells and hepatocytes in a severe combined immunodeficient (SCID) mouse model of amebic liver abscess. By studying infection in C57/BL6.lpr and C57/BL6.gld mice, we found that E. histolytica-induced apoptosis does not require the Fas/Fas ligand pathway of apoptosis, and by using mice with a targeted deletion of the tumor necrosis factor receptor I gene, we have shown that E. histolytica-induced apoptosis is not mediated by tumor necrosis factor alpha. Our data indicate that apoptosis plays a prominent role in the host cell death seen in amebic liver abscess in a mouse model of disease and suggest that E. histolytica induces cell death without using two common pathways for apoptosis.

* Corresponding author. Mailing address: Washington University School of Medicine, 660 S. Euclid Ave., Box 8051, St. Louis, MO 63110. Phone: (314) 362-1071. Fax: (314) 362-3525. E-mail: stanley{at}im.wustl.edu.

Infect Immun, June 1998, p. 2980-2983, Vol. 66, No. 6
0019-9567/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.


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