Hostname: page-component-8448b6f56d-c47g7 Total loading time: 0 Render date: 2024-04-25T01:44:39.831Z Has data issue: false hasContentIssue false

New insights into the functions of anthrax toxin

Published online by Cambridge University Press:  11 April 2006

David J. Banks
Affiliation:
Department of Microbiology, Immunology and Molecular Genetics, 609 Charles E. Young Dr. East, Molecular Sciences Building, University of California at Los Angeles, Los Angeles, CA 90095, USA.
Sabrina C. Ward
Affiliation:
Department of Microbiology, Immunology and Molecular Genetics, 609 Charles E. Young Dr. East, Molecular Sciences Building, University of California at Los Angeles, Los Angeles, CA 90095, USA.
Kenneth A. Bradley
Affiliation:
Department of Microbiology, Immunology and Molecular Genetics, 609 Charles E. Young Dr. East, Molecular Sciences Building, University of California at Los Angeles, Los Angeles, CA 90095, USA.

Abstract

Anthrax is the disease caused by the Gram-positive bacterium Bacillus anthracis. Two toxins secreted by B. anthracis – lethal toxin (LT) and oedema toxin (OT) – contribute significantly to virulence. Although these toxins have been studied for half a century, recent evidence indicates that LT and OT have several roles during infection not previously ascribed to them. Research on toxin-induced effects other than cytolysis of target cells has revealed that LT and OT influence cell types previously thought to be insensitive to toxin. Multiple host factors that confer sensitivity to anthrax toxin have been identified recently, and evidence indicates that the toxins probably contribute to colonisation and invasion of the host. Additionally, the toxins are now known to cause a wide spectrum of tissue and organ pathophysiologies associated with anthrax. Taken together, these new findings indicate that anthrax-toxin-associated pathogenesis is much more complex than has been traditionally recognised.

Type
Review Article
Copyright
© Cambridge University Press 2006

Access options

Get access to the full version of this content by using one of the access options below. (Log in options will check for institutional or personal access. Content may require purchase if you do not have access.)