ArticleMolecular biology of the cell1992
Biochemical and physiological changes induced by anthrax lethal toxin in J774 macrophage-like cells.
Article in Molecular biology of the cell, 1992. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 101 citations in OpenAlex.
- Rational corticosteroids administration and antibiotic treatment is key to managing cutaneous anthrax.BMC infectious diseases · 2024Article
- Anti-proliferative role of recombinant lethal toxin of Bacillus anthracis on primary mammary ductal carcinoma cells revealing its therapeutic potential.Oncotarget · 2017Article
- Soluble Expression and Characterization of Biologically Active Bacillus anthracis Protective Antigen in Escherichia coli.Molecular biology international · 2016Article
- Caspase-1 autoproteolysis is differentially required for NLRP1b and NLRP3 inflammasome function.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Review
- In situ gastrointestinal protection against anthrax edema toxin by single-chain antibody fragment producing lactobacilli.BMC biotechnology · 2011Article
- Anthrax lethal factor activates K(+) channels to induce IL-1β secretion in macrophages.Journal of immunology (Baltimore, Md. : 1950) · 2011Article
- Constitutive MEK1 activation rescues anthrax lethal toxin-induced vascular effects in vivo.Infection and immunity · 2010Article
- Nano aptasensor for protective antigen toxin of anthrax.Analytical chemistry · 2010Article
- Anthrax lethal toxin triggers the formation of a membrane-associated inflammasome complex in murine macrophages.Infection and immunity · 2009Article
- Increased Mitochondrial Activity in Anthrax-Induced Cell Death.Journal of cell death · 2009Article
- ATP Depletion Via Mitochondrial F1F0 Complex by Lethal Factor is an Early Event in B. Anthracis-Induced Sudden Cell Death.Journal of cell death · 2009Article
- Killing of macrophages by anthrax lethal toxin: involvement of the N-end rule pathway.Cellular microbiology · 2008Article
- Anthrax lethal toxin-induced inflammasome formation and caspase-1 activation are late events dependent on ion fluxes and the proteasome.Cellular microbiology · 2008Article
- Neutralizing activity of vaccine-induced antibodies to two Bacillus anthracis toxin components, lethal factor and edema factor.Clinical and vaccine immunology : CVI · 2008Article
- Human monoclonal antibodies against anthrax lethal factor and protective antigen act independently to protect against Bacillus anthracis infection and enhance endogenous immunity to anthrax.Infection and immunity · 2007Article
- Detection of anthrax toxin in the serum of animals infected with Bacillus anthracis by using engineered immunoassays.Clinical and vaccine immunology : CVI · 2006Article
- Glycerol monolaurate inhibits the effects of Gram-positive select agents on eukaryotic cells.Biochemistry · 2006Article
- Neutralizing antibodies and persistence of immunity following anthrax vaccination.Clinical and vaccine immunology : CVI · 2006Article
- GeneChip analyses of global transcriptional responses of murine macrophages to the lethal toxin of Bacillus anthracis.Infection and immunity · 2005Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Experiments were performed to probe the mechanism by which Bacillus anthracis Lethal Toxin (LeTx) causes lysis of J774 macrophage-like cells. After incubation of cells with saturating concentrations of the toxin, two categories of effects were found, which were distinguishable on the basis of chronology, Ca(2+)-dependence, and sensitivity to osmolarity. The earliest events (category I), beginning 45 min postchallenge, were an increase in permeability to 22Na and 86Rb and a rapid conversion of ATP to ADP and AMP. Later events (category II) included alterations in membrane permeability to 45Ca, 51Cr, 36Cl, 35SO4, 3H-amino acids, and 3H-uridine, beginning at 60 min; inhibition of macromolecular synthesis, leakage of cellular lactate dehydrogenase and onset of gross morphological changes, at approximately 75 min; and cell lysis, beginning at 90 min. Category II events exhibited an absolute requirement for extracellular Ca2+ and were blocked by addition of 0.3 M sucrose to the medium, whereas category I events were attenuated, but not blocked, by either of these conditions. On the other hand, both ATP depletion and the category II events were blocked in osmotically stabilized medium that was also isoionic for Na+ and K+. This suggests that permeabilization of the plasma membrane to monovalent cations and water may be the earliest of the physiological changes described here. The resulting influx of Na+ and efflux of K+ would be expected to cause depletion of ATP, via increased activity of the Na+/K+ pump. Subsequently the influx of Ca2+, induced by depletion of ATP, imbalances in monovalent cautions, and/or more dramatic changes in permeability due to influx of water, would be expected to trigger widespread changes leading ultimately to cytolysis.
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