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Development and Functional Characterization of Murine Tolerogenic Dendritic Cells
Published on: May 18, 2018
Anthrax edema toxin sensitizes DBA/2J mice to lethal toxin
Aaron M Firoved1, Mahtab Moayeri, Jason F Wiggins
1National Institute of Allergy and Infectious Diseases, National Institutes of Health, 30 Convent Dr., Building 30, Room 303, Bethesda, MD 20892-4349, USA.
Infection and Immunity
|March 7, 2007
Summary
Edema toxin (ET) causes adrenal lesions and increases corticosterone production even at sublethal doses. Low doses of ET can sensitize mice to lethal toxin (LT), demonstrating synergistic lethality between anthrax toxin components.
Area of Science:
- Toxicology
- Immunology
- Endocrinology
Background:
- Anthrax toxin comprises protective antigen (PA), edema factor (EF), and lethal factor (LF).
- Edema toxin (ET), formed by EF and PA, causes edema and adrenal necrosis at lethal doses.
- Mice resistant to lethal toxin (LT; LF plus PA) can be sensitized by endocrine system perturbation.
Purpose of the Study:
- To investigate the effects of sublethal doses of ET on adrenal glands.
- To determine if sublethal ET can sensitize LT-resistant mice to LT-mediated lethality.
Main Methods:
- Administration of varying doses of ET to BALB/cJ and DBA/2J mice.
- Assessment of adrenal lesions and corticosterone production in ET-treated mice.
- Co-administration or prior administration of ET with LT to DBA/2J mice to evaluate sensitization.
Main Results:
- Sublethal ET doses (10 microg) induced significant adrenal lesions without overt illness.
- ET treatment led to increased, not decreased, corticosterone production.
- Low doses of ET (5 microg) concurrently with LT, or higher doses (15 microg) 18 hours prior, sensitized DBA/2J mice to LT lethality.
Conclusions:
- Sublethal ET induces adrenal damage and alters endocrine function.
- ET can overcome LT resistance in mice, highlighting the synergistic potential of anthrax toxin components in causing severe pathology and death.
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