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PMID: 1457831 Published · ppublish English Journal Article Research Support, U.S. Gov't, P.H.S.

Biochemical and physiological changes induced by anthrax lethal toxin in J774 macrophage-like cells.

Molecular biology of the cell ·Vol. 3 ·No. 11 ·1992-11-00 ·Pages 1269-77

Hanna PC, Kochi S, Collier RJ

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.

MeSH Terms
Adenosine Diphosphate/metabolism Adenosine Monophosphate/metabolism Adenosine Triphosphate/metabolism Antigens, Bacterial Bacillus anthracis Bacterial Toxins/toxicity Calcium/metabolism Cell Line Cell Membrane Permeability/drug effects Macrophages/drug effects,metabolism,physiology Osmolar Concentration
Chemicals
Antigens, Bacterial Bacterial Toxins anthrax toxin Adenosine Monophosphate Adenosine Diphosphate Adenosine Triphosphate Calcium
Authors & Affiliations
3 authors, click to expand affiliations / ORCID
Hanna P C
Department of Microbiology and Molecular Genetics, Harvard Medical School, Boston, Massachusetts 02115.
Kochi S
Collier R J
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Article Info
Journal
Molecular biology of the cell
Abbr.
Mol Biol Cell
ISSN
1059-1524
Published
1992-11-00
Pages
1269-77
Language
English
Region
United States
NLM ID
9201390
PMCID
PMC275693
Subset
IM
Grants
NIAID NIH HHS · AI-22021 · United States
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