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- Title
Antiplatelet Activities of Anthrax Lethal Toxin Are Associated with Suppressed p42/44 and p38 Mitogen-Activated Protein Kinase Pathways in the Platelets.
- Authors
Jyh-Hwa Kau; Der-Shan Sun; Wei-Jern Tsai; Huey-Fen Shyu; Hsin-Hsien Huang; Hung-Chi Lin; Hsin-Hou Chang
- Abstract
Anthrax lethal toxin (LT) is the major virulence factor produced by Bacillus anthracis, but the mechanism by which it induces high mortality remains unclear. We found that LT treatment could induce severe hemorrhage in mice and significantly suppress human whole-blood dotting and platelet aggregation in vitro. In addition, LT could inhibit agonist-induced platelet surface P-selectin expression, resulting in the inhibition of platelet-endothelial cell engagements. Data from Western blot analysis indicated that LT treatment resulted in the suppression of p42/44 and p38 mitogen-activated protein kinase pathways in platelets. Combined treatments with LT and antiplatelet agents such as aspirin and the RGD-containing disintegrin rhodostomin significantly increased mortality in mice. Our data suggest that platelets are a pathogenic target for anthrax LT.
- Publication
Journal of Infectious Diseases, 2005, Vol 192, Issue 8, p1465
- ISSN
0022-1899
- Publication type
Academic Journal
- DOI
10.1086/491477