Nalp1b controls mouse macrophage susceptibility to anthrax lethal toxin

The pathogenesis of Bacillus anthracis, the bacterium that causes anthrax, depends on secretion of three factors that combine to form two bipartite toxins. Edema toxin, consisting of protective antigen (PA) and edema factor (EF), causes the edema associated with cutaneous anthrax infections, whereas...

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Published inNature genetics Vol. 38; no. 2; pp. 240 - 244
Main Authors Dietrich, William F, Boyden, Eric D
Format Journal Article
LanguageEnglish
Published New York Nature Publishing Group US 01.02.2006
Nature Publishing Group
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Abstract The pathogenesis of Bacillus anthracis, the bacterium that causes anthrax, depends on secretion of three factors that combine to form two bipartite toxins. Edema toxin, consisting of protective antigen (PA) and edema factor (EF), causes the edema associated with cutaneous anthrax infections, whereas lethal toxin (LeTx), consisting of PA and lethal factor (LF), is believed to be responsible for causing death in systemic anthrax infections. EF and LF can be transported by PA into the cytosol of many cell types. In mouse macrophages, LF can cause rapid necrosis that may be related to the pathology of systemic infections. Inbred mouse strains display variable sensitivity to LeTx-induced macrophage necrosis. This trait difference has been mapped to a locus on chromosome 11 named Ltxs1 (refs. 7,8). Here we show that an extremely polymorphic gene in this locus, Nalp1b, is the primary mediator of mouse macrophage susceptibility to LeTx. We also show that LeTx-induced macrophage death requires caspase-1, which is activated in susceptible, but not resistant, macrophages after intoxication, suggesting that Nalp1b directly or indirectly activates caspase-1 in response to LeTx.
AbstractList The pathogenesis of Bacillus anthracis, the bacterium that causes anthrax, depends on secretion of three factors that combine to form two bipartite toxins. Edema toxin, consisting of protective antigen (PA) and edema factor (EF), causes the edema associated with cutaneous anthrax infections, whereas lethal toxin (LeTx), consisting of PA and lethal factor (LF), is believed to be responsible for causing death in systemic anthrax infections super(1). EF and LF can be transported by PA into the cytosol of many cell types super(2). In mouse macrophages, LF can cause rapid necrosis that may be related to the pathology of systemic infections super(3, ) super(4, ) super(5). Inbred mouse strains display variable sensitivity to LeTx-induced macrophage necrosis super(6, ) super(7). This trait difference has been mapped to a locus on chromosome 11 named Ltxs1 (refs. 7,8). Here we show that an extremely polymorphic gene in this locus, Nalp1b, is the primary mediator of mouse macrophage susceptibility to LeTx. We also show that LeTx-induced macrophage death requires caspase-1, which is activated in susceptible, but not resistant, macrophages after intoxication, suggesting that Nalp1b directly or indirectly activates caspase-1 in response to LeTx.
The pathogenesis of Bacillus anthracis , the bacterium that causes anthrax, depends on secretion of three factors that combine to form two bipartite toxins. Edema toxin, consisting of protective antigen (PA) and edema factor (EF), causes the edema associated with cutaneous anthrax infections, whereas lethal toxin (LeTx), consisting of PA and lethal factor (LF), is believed to be responsible for causing death in systemic anthrax infections 1 . EF and LF can be transported by PA into the cytosol of many cell types 2 . In mouse macrophages, LF can cause rapid necrosis that may be related to the pathology of systemic infections 3 , 4 , 5 . Inbred mouse strains display variable sensitivity to LeTx-induced macrophage necrosis 6 , 7 . This trait difference has been mapped to a locus on chromosome 11 named Ltxs1 (refs. 7 , 8 ). Here we show that an extremely polymorphic gene in this locus, Nalp1b , is the primary mediator of mouse macrophage susceptibility to LeTx. We also show that LeTx-induced macrophage death requires caspase-1, which is activated in susceptible, but not resistant, macrophages after intoxication, suggesting that Nalp1b directly or indirectly activates caspase-1 in response to LeTx.
The pathogenesis of Bacillus anthracis, the bacterium that causes anthrax, depends on secretion of three factors that combine to form two bipartite toxins. Edema toxin, consisting of protective antigen (PA) and edema factor (EF), causes the edema associated with cutaneous anthrax infections, whereas lethal toxin (LeTx), consisting of PA and lethal factor (LF), is believed to be responsible for causing death in systemic anthrax infections. EF and LF can be transported by PA into the cytosol of many cell types. In mouse macrophages, LF can cause rapid necrosis that may be related to the pathology of systemic infections. Inbred mouse strains display variable sensitivity to LeTx-induced macrophage necrosis. This trait difference has been mapped to a locus on chromosome 11 named Ltxs1 (refs. 7,8). Here we show that an extremely polymorphic gene in this locus, Nalp1b, is the primary mediator of mouse macrophage susceptibility to LeTx. We also show that LeTx-induced macrophage death requires caspase-1, which is activated in susceptible, but not resistant, macrophages after intoxication, suggesting that Nalp1b directly or indirectly activates caspase-1 in response to LeTx.
Audience Academic
Author Dietrich, William F
Boyden, Eric D
Author_xml – sequence: 1
  givenname: William F
  surname: Dietrich
  fullname: Dietrich, William F
  organization: Department of Genetics, Harvard Medical School
– sequence: 2
  givenname: Eric D
  surname: Boyden
  fullname: Boyden, Eric D
  organization: Department of Genetics, Harvard Medical School
BackLink http://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=17664862$$DView record in Pascal Francis
https://www.ncbi.nlm.nih.gov/pubmed/16429160$$D View this record in MEDLINE/PubMed
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IngestDate Wed Dec 04 08:01:55 EST 2024
Tue Nov 19 05:01:59 EST 2024
Tue Nov 19 21:44:24 EST 2024
Wed Nov 13 00:05:21 EST 2024
Sat Sep 28 21:00:33 EDT 2024
Sat Sep 28 21:04:52 EDT 2024
Fri Dec 06 02:40:28 EST 2024
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Sun Oct 22 16:06:57 EDT 2023
Thu Dec 12 04:11:25 EST 2024
Thu Oct 07 19:38:52 EDT 2021
IsPeerReviewed true
IsScholarly true
Issue 2
Keywords Infection
Toxin
Vertebrata
Regulation(control)
Mammalia
Mouse
Anthrax
Rodentia
Bacteriosis
Macrophage
Language English
License CC BY 4.0
http://www.springer.com/tdm
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SO Kim (BFng1724_CR24) 2003; 278
BJ Geddes (BFng1724_CR16) 2001; 284
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SSID ssj0014408
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Snippet The pathogenesis of Bacillus anthracis, the bacterium that causes anthrax, depends on secretion of three factors that combine to form two bipartite toxins....
The pathogenesis of Bacillus anthracis , the bacterium that causes anthrax, depends on secretion of three factors that combine to form two bipartite toxins....
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StartPage 240
SubjectTerms Agriculture
Alleles
Animal Genetics and Genomics
Animals
Anthrax
Antigens, Bacterial - toxicity
Apoptosis Regulatory Proteins - antagonists & inhibitors
Apoptosis Regulatory Proteins - metabolism
Bacillus anthracis
Bacterial toxins
Bacterial Toxins - toxicity
Base Sequence
Biological and medical sciences
Biomedical and Life Sciences
Biomedicine
Cancer Research
Caspase 1 - metabolism
Cell Survival
Cellular biology
Complications and side effects
Diagnosis
Disease Susceptibility
Edema
Enzymes
Exons - genetics
Fundamental and applied biological sciences. Psychology
Gene Function
Gene loci
Genetic aspects
Genetics of eukaryotes. Biological and molecular evolution
Genomics
Human Genetics
letter
Macrophages
Macrophages - drug effects
Macrophages - metabolism
Macrophages - pathology
Mice
Mice, Transgenic
Molecular Sequence Data
Mortality
Pathology
Physiological aspects
Polymorphism, Genetic
Risk factors
RNA, Messenger - genetics
RNA, Messenger - metabolism
Rodents
Toxins
Title Nalp1b controls mouse macrophage susceptibility to anthrax lethal toxin
URI http://dx.doi.org/10.1038/ng1724
https://link.springer.com/article/10.1038/ng1724
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Volume 38
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