Evidence map›Paper›PMID 15972515›Full record

ArticleInfection and immunity2005

Endocrine perturbation increases susceptibility of mice to anthrax lethal toxin.

Mahtab Moayeri, Jeanette I Webster, Jason F Wiggins, Stephen H Leppla, Esther M Sternberg

Open access · greenAbstract read
In one paragraph

Article in Infection and immunity, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.8field-weighted citation impact, top 16% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

19 citing papers in PubMed, 37 citations in OpenAlex.

  1. Review
  2. Anthrax and the inflammasome.Microbes and infection · 2012
    Review
  3. Review
  4. Cellular and physiological effects of anthrax exotoxin and its relevance to disease.Frontiers in cellular and infection microbiology · 2012
    Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. Pathophysiology of anthrax.Frontiers in bioscience (Landmark edition) · 2009
    Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 1 country.

Mahtab MoayeriMcrobial Pathogenesis Section, National Institute of Allergy and Infectious Diseases, Building 30, Room 303, National Institutes of Health, Bethesda, Maryland 20892, USA. mmoayeri@niaid.nih.gov
Jeanette I Webster
Jason F Wiggins
Stephen H Leppla
Esther M Sternberg
National Institutes of Health · USNational Institute of Allergy and Infectious Diseases · US

Funding

Vaccines and Therapeutics for AnthraxZIAAI000929 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI LEPPLA, STEPHEN · 2009 to 2025
$15.9M
Role of Neuroendocrine Stress Response in Inflammatory and Behavioral Illness.ZIAMH002585 · NIMH · NATIONAL INSTITUTE OF MENTAL HEALTH · PI STERNBERG, ESTHER M. · 2009 to 2012
$7.3M
Vaccines and Therapeutics for AnthraxZ01AI000929 · NIAID · NIAID EXTRAMURAL ACTIVITIES · PI LEPPLA, STEPHEN H · 2003 to 2008
$6.7M
ROLE OF THE CNS IN THE SUSCEPTIBILITY TO INFLAMMATORY ILLNESSZ01MH002585 · NIMH · NATIONAL INSTITUTE OF MENTAL HEALTH · PI STERNBERG, ESTHER M. · 1991 to 2008
$3.7M
6 · The paper itself

Abstract

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.

Indexed as

AdrenalectomyAldosteroneAnimalsAntigens, BacterialBacterial ToxinsCorticosteroneCytokinesDexamethasoneHypothalamo-Hypophyseal SystemMacrophagesMaleMiceMice, Inbred BALB CMice, Inbred C57BLMice, Inbred DBAPituitary-Adrenal SystemAldosteroneanthrax toxinAntigens, BacterialBacterial ToxinsCorticosteroneCytokinesDexamethasoneReceptors, Glucocorticoid

Identifiers

PMID15972515
PMCPMC1168625
OpenAlexW2096313446

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.