|  Help  |  About  |  Contact Us

Publication : Epithelial cell apoptosis facilitates Entamoeba histolytica infection in the gut.

First Author  Becker SM Year  2010
Journal  Am J Pathol Volume  176
Issue  3 Pages  1316-22
PubMed ID  20093500 Mgi Jnum  J:158351
Mgi Id  MGI:4438643 Doi  10.2353/ajpath.2010.090740
Citation  Becker SM, et al. (2010) Epithelial cell apoptosis facilitates Entamoeba histolytica infection in the gut. Am J Pathol 176(3):1316-22
abstractText  Entamoeba histolytica is the protozoan parasite that causes amebic colitis. The parasite triggers apoptosis on contact with host cells; however, the biological significance of this event during intestinal infection is unclear. We examined the role of apoptosis in a mouse model of intestinal amebiasis. Histopathology revealed that abundant epithelial cell apoptosis occurred in the vicinity of amoeba in histological specimens. Epithelial cell apoptosis occurred rapidly on co-culture with amoeba in vitro as measured by annexin positivity, DNA degradation, and mitochondrial dysfunction. Administration of the pan caspase inhibitor ZVAD decreased the rate and severity of amebic infection in CBA mice by all measures (cecal culture positivity, parasite enzyme-linked immunosorbent assay, and histological scores). Similarly, caspase 3 knockout mice on the resistant C57BL/6 background exhibited even lower cecal parasite antigen burden and culture positive rates than wild type mice. The permissive effect of apoptosis on infection could be tracked to the epithelium, in that transgenic mice that overexpressed Bcl-2 in epithelial cells were more resistant to infection as measured by cecal parasite enzyme-linked immunosorbent assay and histological scores. We concluded that epithelial cell apoptosis in the intestine facilitates amebic infection in this mouse model. The parasite's strategy for inducing apoptosis may point to key virulence factors, and therapeutic maneuvers to diminish epithelial apoptosis may be useful in amebic colitis.
Quick Links:
 
Quick Links:
 

Expression

Publication --> Expression annotations

 

Other

6 Bio Entities

Trail: Publication

0 Expression