Key tissue targets responsible for anthrax-toxin-induced lethality

Shihui Liu (), Yi Zhang, Mahtab Moayeri, Jie Liu, Devorah Crown, Rasem J. Fattah, Alexander N. Wein, Zu-Xi Yu, Toren Finkel and Stephen H. Leppla ()
Additional contact information
Shihui Liu: Microbial Pathogenesis Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health
Yi Zhang: Microbial Pathogenesis Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health
Mahtab Moayeri: Microbial Pathogenesis Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health
Jie Liu: Center for Molecular Medicine, National Heart, Lung, and Blood Institute, National Institutes of Health
Devorah Crown: Microbial Pathogenesis Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health
Rasem J. Fattah: Microbial Pathogenesis Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health
Alexander N. Wein: Microbial Pathogenesis Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health
Zu-Xi Yu: Pathology Core Facility, National Heart, Lung, and Blood Institute, National Institutes of Health
Toren Finkel: Center for Molecular Medicine, National Heart, Lung, and Blood Institute, National Institutes of Health
Stephen H. Leppla: Microbial Pathogenesis Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health

Nature, 2013, vol. 501, issue 7465, 63-68

Abstract: Abstract Bacillus anthracis, the causative agent of anthrax disease, is lethal owing to the actions of two exotoxins: anthrax lethal toxin (LT) and oedema toxin (ET). The key tissue targets responsible for the lethal effects of these toxins are unknown. Here we generated cell-type-specific anthrax toxin receptor capillary morphogenesis protein-2 (CMG2)-null mice and cell-type-specific CMG2-expressing mice and challenged them with the toxins. Our results show that lethality induced by LT and ET occurs through damage to distinct cell types; whereas targeting cardiomyocytes and vascular smooth muscle cells is required for LT-induced mortality, ET-induced lethality occurs mainly through its action in hepatocytes. Notably, and in contradiction to what has been previously postulated, targeting of endothelial cells by either toxin does not seem to contribute significantly to lethality. Our findings demonstrate that B. anthracis has evolved to use LT and ET to induce host lethality by coordinately damaging two distinct vital systems.

Date: 2013
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DOI: 10.1038/nature12510

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