ArticleProceedings of the National Academy of Sciences of the United States of America2003
Toxin-induced resistance in Bacillus anthracis lethal toxin-treated macrophages.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 42 citations in OpenAlex.
- HDAC8 Prevents Anthrax Lethal Toxin-induced Cell Cycle Arrest through Silencing PTEN in Human Monocytic THP-1 Cells.Toxins · 2017Article
- HDAC8-mediated epigenetic reprogramming plays a key role in resistance to anthrax lethal toxin-induced pyroptosis in macrophages.Journal of immunology (Baltimore, Md. : 1950) · 2014Article
- Platelet-activating factor contributes to Bacillus anthracis lethal toxin-associated damage.The Journal of biological chemistry · 2014Article
- Cellular adaptation to anthrax lethal toxin-induced mitochondrial cholesterol enrichment, hyperpolarization, and reactive oxygen species generation through downregulating MLN64 in macrophages.Molecular and cellular biology · 2012Article
- Serum amyloid A protects murine macrophages from lethal toxin-mediated death.Cellular immunology · 2012Article
- Targeting the brain with PEG-PLGA nanoparticles modified with phage-displayed peptides.Biomaterials · 2011Article
- Noninvasive imaging technologies reveal edema toxin as a key virulence factor in anthrax.The American journal of pathology · 2011Article
- Serum response factor regulates immediate early host gene expression in Toxoplasma gondii-infected host cells.PloS one · 2011Article
- Cellular and systemic effects of anthrax lethal toxin and edema toxin.Molecular aspects of medicine · 2009Review
- Anthrax lethal toxin induced lysosomal membrane permeabilization and cytosolic cathepsin release is Nlrp1b/Nalp1b-dependent.PloS one · 2009Article
- Heat shock inhibits caspase-1 activity while also preventing its inflammasome-mediated activation by anthrax lethal toxin.Cellular microbiology · 2008Article
- Toxoplasma gondii rhoptry discharge correlates with activation of the early growth response 2 host cell transcription factor.Infection and immunity · 2008Article
- Article
- Acceleration of epithelial cell syndecan-1 shedding by anthrax hemolytic virulence factors.BMC microbiology · 2006Article
- Anthrax lethal toxin-mediated killing of human and murine dendritic cells impairs the adaptive immune response.PLoS pathogens · 2005Article
- Binary bacterial toxins: biochemistry, biology, and applications of common Clostridium and Bacillus proteins.Microbiology and molecular biology reviews : MMBR · 2004Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
In the current study, we show that macrophages adaptively resist anthrax lethal toxin (LT) through a toxin-activated process termed toxin-induced resistance (TIR). TIR was triggered by pretreatment of RAW 264.7 or J774A.1 macrophages with a low dose of LT for at least 6 h, which resulted in resistance to high doses of LT for 96 h. Activation of TIR required functional toxin, because LT subunits, mutants, and heat-inactivated toxin were unable to trigger resistance. TIR macrophages were not altered in toxin receptor levels or cell cycle profiles. Treatment of TIR macrophages with high doses of LT resulted in a sustained decline in full-length mitogen-activated protein kinase kinase 2, a known target of lethal factor, and a marked reduction in diphosphorylated extracellular response kinases 1,2 for 24 h. However, despite the sustained loss of full-length mitogen-activated protein kinase kinase 2, by 48 h, TIR macrophages regained diphosphorylated extracellular response kinases 1,2, suggesting an adaptation led to recovery of this signaling pathway. TIR macrophages were also able to maintain normal levels of ubiquitinylated proteins, whereas sensitive cells show a rapid reduction in ubiquitin-modified proteins before cell death, indicating a possible alteration in proteasome activity contributed to resistance. These results provide a paradigm for toxin-cell interactions and suggest macrophages are capable of adapting to and tolerating toxic doses of LT.
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