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Bacillus anthracis
About: Bacillus anthracis is a research topic. Over the lifetime, 3994 publications have been published within this topic receiving 128122 citations.
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TL;DR: 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.
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. Cell-type-specific anthrax toxin receptor CMG2-null mice are generated and used to show that the Bacillus anthracis toxins lethal toxin (LT) and oedema toxin (ET) target distinct cell types; in contrast to previous suggestions, it is shown that endothelial cells are not key targets for either toxin and instead LT targets cardiomyocytes and vascular smooth muscle cells whereas ET targets hepatocytes. Bacillus anthracis produces two toxins — anthrax lethal toxin and oedema toxin — which are targeted to tissues by captor-associated protective antigen. The two toxins have essential but little understood roles in pathogenesis. Here, Shihui Liu and colleagues generate mice lacking cell-type-specific anthrax toxin receptor capillary morphogenesis protein-2 (CMG2) and use them to show that the two toxins target distinct cell types. Contrary to previous suggestions, endothelial cells are not key targets for either toxin. Rather, lethal toxin targets cardiomyocytes and vascular smooth muscle cells, and oedema toxin targets hepatocytes. Recognition that the anthrax toxins are specifically targeting the cardiovascular system and liver may suggest supportive therapies that would limit tissue damage and increase survival in human anthrax infections.
100 citations
TL;DR: It is found that, in the blood of infected animals, the protective antigen exists primarily as a 63 kDa protein and appears to be complexed with the lethal factor component of the toxin.
Abstract: Summary: The protective antigen component of anthrax lethal toxin, produced in vitro, has a molecular mass of 83 kDa. Cell-culture studies by others have demonstrated that upon binding of the 83 kDa protective antigen to cell-surface receptors, the protein is cleaved by an unidentified cell-associated protease activity. The resultant 63 kDa protein then binds lethal factor to form lethal toxin, which has been proposed to be internalized by endocytosis. We found that, in the blood of infected animals, the protective antigen exists primarily as a 63 kDa protein and appears to be complexed with the lethal factor component of the toxin. Conversion of protective antigen from 83 to 63 kDa was catalysed by a calcium-dependent, heat-labile serum protease. Except for being complexed to protective antigen, there was no apparent alteration of lethal factor during the course of anthrax infection. The protective antigen-cleaving protease appeared to be ubiquitous among a wide range of animal species, including primates, horses, goats, sheep, dogs, cats and rodents.
100 citations
TL;DR: Ratiometric fluorescent detection of anthrax spores can be achieved through the displacement of a different sensitizer by DPA, and lanthanide (Ln3+)-based luminescent detection of DPA has been most promising owing to the unique photophysical properties of Ln3-DPA chelates.
Abstract: Anthrax is an acute disease, concurrently a potential biological warfare agent caused by Bacillus Anthracis. The accurate, rapid, sensitive, and selective detection of Bacillus spores plays a vital role in order to prevent a biological attack or outbreak of disease. Bacterial spores contain a main core cell which is enclosed by protective layers. As a major component of these protective layers, bacterial spores contain up to 1 M dipicolinic acid (DPA), accounting for 5−15 % of the dry mass of the bacterial spore. Hence, DPA is a convenient biomarker for these spores. In recent years a number of biological and chemical detection methods for Bacillus Anthracis spores have been investigated. Biological methods are based on polymerase chain reactions and immunoassays. Important chemical methods employ vibrational spectroscopy (FT-IR, Raman and SERS) and photoluminescence. Among them, lanthanide (Ln3+)-based luminescent detection of DPA has been most promising owing to the unique photophysical properties of Ln3+-DPA chelates, including their bright luminescence upon sensitization by DPA, the long luminescence lifetimes compared to free Ln3+, and the concomitantly high luminescence enhancement ratio upon coordination of DPA to the Ln3+ center. Besides the use of DPA itself as a sensitizer, ratiometric fluorescent detection of anthrax spores can be achieved through the displacement of a different sensitizer by DPA.
100 citations
TL;DR: In this article, an acoustic Love-wave biosensor was used for detection of Bacillus anthracis simulant, Bacillus thuringiensis at or below inhalational infectious levels.
99 citations
TL;DR: The transfer of plasmids by mating from four Bacillus thuringiensis subspecies to Bacillus anthracis and Bacillus cereus recipients was monitored by selecting transcipients which acquired plasmid pBC16 (Tcr), and DNA-DNA hybridization experiments suggested that DNA homology exists among pXO13, pX o14, and pXo16.
Abstract: The transfer of plasmids by mating from four Bacillus thuringiensis subspecies to Bacillus anthracis and Bacillus cereus recipients was monitored by selecting transcipients which acquired plasmid pBC16 (Tcr). Transcipients also inherited a specific large plasmid from each B. thuringiensis donor at a high frequency along with a random array of smaller plasmids. The large plasmids (ca. 50 to 120 megadaltons), pXO13, pXO14, pXO15, and pXO16, originating from B. thuringiensis subsp. morrisoni, B. thuringiensis subsp. toumanoffi, B. thuringiensis subsp. alesti, and B. thuringiensis subsp. israelensis, respectively, were demonstrated to be responsible for plasmid mobilization. Transcipients containing any of the above plasmids had donor capability, while B. thuringiensis strains cured of each of them were not fertile, indicating that the plasmids confer conjugation functions. Confirmation that pXO13, pXO14, and pXO16 were self-transmissible was obtained by the isolation of fertile B. anthracis and B. cereus transcipients that contained only pBC16 and one of these plasmids. pXO14 was efficient in mobilizing the toxin and capsule plasmids, pXO1 and pXO2, respectively, from B. anthracis transcipients to plasmid-cured B. anthracis or B. cereus recipients. DNA-DNA hybridization experiments suggested that DNA homology exists among pXO13, pXO14, and the B. thuringiensis subsp. thuringiensis conjugative plasmids pXO11 and pXO12. Matings performed between strains which each contained the same conjugative plasmid demonstrated reduced efficiency of pBC16 transfer. However, in many instances when donor and recipient strains contained different conjugative plasmids, the efficiency of pBC16 transfer appeared to be enhanced.
99 citations