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Infection and Immunity, July 2005, p. 4238-4244, Vol. 73, No. 7
0019-9567/05/$08.00+0     doi:10.1128/IAI.73.7.4238-4244.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Endocrine Perturbation Increases Susceptibility of Mice to Anthrax Lethal Toxin

Mahtab Moayeri,1* Jeanette I. Webster,2 Jason F. Wiggins,1 Stephen H. Leppla,1 and Esther M. Sternberg2

Microbial Pathogenesis Section, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892,1 Section on Neuroendocrine Immunology and Behavior, National Institute of Mental Health, National Institutes of Health, Bethesda, Maryland 208922

Received 30 December 2004/ Returned for modification 12 February 2005/ Accepted 26 February 2005

Bacillus anthracis lethal toxin (LT) causes vascular collapse and high lethality in BALB/cJ mice, intermediate lethality in C57BL/6J mice, and no lethality in DBA/2J mice. We found that adrenalectomized (ADX) mice of all three strains had increased susceptibility to LT. The increased susceptibility of ADX-DBA/2J mice was not accompanied by changes in their macrophage sensitivity or cytokine response to LT. DBA/2J mice showed no change in serum corticosteroid levels in response to LT injection, while BALB/cJ mice showed a fivefold increase in serum corticosterone. However, LT inhibited dexamethasone (DEX)-induced glucocorticoid receptor gene activation to similar extents in all three strains. DEX treatment did not rescue ADX mice from LT-mediated mortality. Surprisingly, oral DEX treatment also sensitized adrenally intact DBA/2J mice to LT lethality at all doses tested and also exacerbated LT-mediated pathogenesis and mortality in BALB/cJ mice. Aldosterone did not protect ADX mice from toxin challenge. These results indicate that susceptibility to anthrax LT in mice depends on a fine but easily perturbed balance of endocrine functions. Thus, the potentially detrimental consequences of steroid therapy for anthrax must be considered in treatment protocols for this disease.

* Corresponding author. Mailing address: Building 30, Room 303, National Institutes of Health, Bethesda, MD 20892. Phone: (301) 496-1821. Fax: (301) 480-0326. E-mail: mmoayeri{at}niaid.nih.gov.

Editor: J. D. Clements

Infection and Immunity, July 2005, p. 4238-4244, Vol. 73, No. 7
0019-9567/05/$08.00+0     doi:10.1128/IAI.73.7.4238-4244.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.



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