Anthrax toxin edema factor: a bacterial adenylate cyclase that increases cyclic AMP concentrations of eukaryotic cells.
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It is shown here that EF is an adenylate cyclase [ATP pyrophosphate-lyase (cyclizing), EC 4.6.1] produced by Bacillus anthracis in an inactive form and nearly equals that of the most active known cyclase.Abstract:
Anthrax toxin is composed of three proteins: protective antigen (PA), lethal factor (LF), and edema factor (EF). These proteins individually cause no known physiological effects in animals but in pairs produce two toxic actions. Injection of PA with LF causes death of rats in 60 min, whereas PA with EF causes edema in the skin of rabbits and guinea pigs. The mechanisms of action of these proteins have not been determined. It is shown here that EF is an adenylate cyclase [ATP pyrophosphate-lyase (cyclizing), EC 4.6.1.1] produced by Bacillus anthracis in an inactive form. Activation occurs upon contact with a heat-stable eukaryotic cell material. The specific activity of the resulting adenylate cyclase nearly equals that of the most active known cyclase. In Chinese hamster ovary cells exposed to PA and EF, cAMP concentrations increase without a lag to values about 200-fold above normal, remain high in the continued presence of toxin, and decrease rapidly after its removal. The increase in cAMP is completely blocked by excess LF. It is suggested that PA interacts with cells to form a receptor system by which EF and perhaps LF gain access to the cytoplasm.read more
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Journal ArticleDOI
Structural Integrity of the Alveolar-Capillary Barrier in Cynomolgus Monkeys Challenged with Fully Virulent and Toxin-Deficient Strains of Bacillus anthracis.
TL;DR: Structural integrity of the alveolar capillary barrier in archival formalin-fixed lungs of cynomolgus monkeys challenged with the fully virulent B. anthracis Ames wild-type strain or the isogenic toxin-deficient mutants ΔEF, ΔLF, and ΔPA is examined to provide evidence that LT plays a determinative role in bacterial dissemination and alveolars-capillary barrier dysfunction while ET may significantly exacerbate pulmonary pathologies in a systemic infection.
Journal ArticleDOI
Passive Immunotherapy Protects against Enteric Invasion and Lethal Sepsis in a Murine Model of Gastrointestinal Anthrax
TL;DR: It is demonstrated that passive immunotherapy with anti-anthrax PA mAb, administered at the same time as gastrointestinal exposure to B. anthracis, prevents lethal sepsis in nearly all cases, while a delay of up to forty-eight hours in treatment still greatly reduces mortality following exposure (65%).
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Protective immunity induced by Bacillus anthracis toxin mutant strains.
TL;DR: Bacillus anthracis is the etiological agent of anthrax, a disease often fatal in humans and many animals species, and it has been suggested that LF is a metalloprotease (Klimpel et al., 1994).
Book ChapterDOI
Inhibitors of pore-forming toxins
TL;DR: The focus of this chapter is on the biophysical studies of channel-forming bacterial toxins that suggest new approaches to block their virulent action, and the constructive role of the attractive interaction between the channel and blocker molecules is addressed.
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