Where and how do anthrax toxins exit endosomes to intoxicate host cells?

Trends Microbiol

Dipartimento di Scienze Biomediche Sperimentali, Università di Padova, viale G. Colombo 3, I-35121 Padua, Italy.

Published: November 2007

The role of Bacillus anthracis virulence factors in its pathogenesis has been subjected to intense investigation with the aim of finding novel preventive and therapeutic protocols. Toxins that are endocytosed and act in the cytosol of host cells have a central role in B. anthracis infection. Understanding of anthrax toxin cell entry has increased during the past few years and a composite picture is emerging. Nevertheless, unanswered and controversial questions remain, particularly concerning the site and mode of anthrax toxin cell entry, the role of anthrax toxin receptors in the process and the possible involvement of cytosolic chaperones, which might affect entry efficiency. Here, the current model of anthrax toxin cell entry, an alternative model and experimental approaches for clarifying unanswered questions will be discussed.

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.tim.2007.10.003DOI Listing

Publication Analysis

Top Keywords

anthrax toxin
16
toxin cell
12
cell entry
12
anthrax
5
anthrax toxins
4
toxins exit
4
exit endosomes
4
endosomes intoxicate
4
intoxicate host
4
host cells?
4

Similar Publications

MAP Kinase Signaling at the Crossroads of Inflammasome Activation.

Immunol Rev

January 2025

Department of Internal Medicine and Paediatrics, Ghent University, Ghent, Belgium.

Inflammasomes are crucial mediators of both antimicrobial host defense and inflammatory pathology, requiring stringent regulation at multiple levels. This review explores the pivotal role of mitogen-activated protein kinase (MAPK) signaling in modulating inflammasome activation through various regulatory mechanisms. We detail recent advances in understanding MAPK-mediated regulation of NLRP3 inflammasome priming, licensing and activation, with emphasis on MAPK-induced activator protein-1 (AP-1) signaling in NLRP3 priming, ERK1 and JNK in NLRP3 licensing, and TAK1 in connecting death receptor signaling to NLRP3 inflammasome activation.

View Article and Find Full Text PDF

Bacillus cereus biovar anthracis (Bcbva) causes anthrax-like disease in animals, particularly in the non-human primates and great apes of West and Central Africa. Genomic analyses revealed Bcbva as a member of the B. cereus species that carries two plasmids, pBCXO1 and pBCXO2, which have high sequence homology to the B.

View Article and Find Full Text PDF

Comparing microbiological and molecular diagnostic tools for the surveillance of anthrax.

PLoS Negl Trop Dis

November 2024

Department of Veterinary Tropical Diseases, Faculty of Veterinary Science, University of Pretoria, Onderstepoort, South Africa.

The diagnosis of anthrax, a zoonotic disease caused by Bacillus anthracis can be complicated by detection of closely related species. Conventional diagnosis of anthrax involves microscopy, culture identification of bacterial colonies and molecular detection. Genetic markers used are often virulence gene targets such as B.

View Article and Find Full Text PDF

Hyaline fibromatosis syndrome is a rare, progressive and fatal autosomal recessive disorder characterised by multiple subcutaneous skin nodules, osteopenia, joint contractures, failure to thrive, diarrhoea and frequent infections. There is diffuse deposition of hyaline material in the skin, gastrointestinal tract, muscle and endocrine glands. The disease is often underdiagnosed since infants affected with the disease pass away early prior to establishing a final diagnosis.

View Article and Find Full Text PDF

causes anthrax through a combination of bacterial infection and toxemia. As a major virulence factor of , anthrax lethal toxin (LT) is a zinc-dependent metalloproteinase, exerting its cytotoxicity through proteolytic cleavage of the mitogen-activated protein kinase kinases, thereby shutting down the MAPK pathways. Anthrax lethal toxin induces host lethality mostly by targeting the cardiovascular system.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!