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Research Article

Inflammasome Sensor Nlrp1b-Dependent Resistance to Anthrax Is Mediated by Caspase-1, IL-1 Signaling and Neutrophil Recruitment

  • Mahtab Moayeri,

    Affiliation: Laboratory of Bacterial Diseases, Bacterial Toxins and Therapeutics Section, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, United States of America

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  • Devorah Crown,

    Affiliation: Laboratory of Bacterial Diseases, Bacterial Toxins and Therapeutics Section, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, United States of America

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  • Zachary L. Newman,

    Affiliation: Laboratory of Bacterial Diseases, Bacterial Toxins and Therapeutics Section, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, United States of America

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  • Shu Okugawa,

    Affiliation: Laboratory of Bacterial Diseases, Bacterial Toxins and Therapeutics Section, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, United States of America

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  • Michael Eckhaus,

    Affiliation: Diagnostic and Research Services Branch, Division of Veterinary Resources, Office of Research Services, National Institutes of Health, Bethesda, Maryland, United States of America

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  • Christophe Cataisson,

    Affiliation: Laboratory of Cancer Biology and Genetics, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, United States of America

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  • Shihui Liu,

    Affiliation: Laboratory of Bacterial Diseases, Bacterial Toxins and Therapeutics Section, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, United States of America

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  • Inka Sastalla,

    Affiliation: Laboratory of Bacterial Diseases, Bacterial Toxins and Therapeutics Section, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, United States of America

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  • Stephen H. Leppla mail

    sleppla@niaid.nih.gov

    Affiliation: Laboratory of Bacterial Diseases, Bacterial Toxins and Therapeutics Section, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, United States of America

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  • Published: December 09, 2010
  • DOI: 10.1371/journal.ppat.1001222

Reader Comments (1)

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Route of infection question

Posted by spopov on 04 Jan 2011 at 22:47 GMT

It is not clear why did the authors chose to use the s.c. route of challenge known to mainly bypass the initial phagocytic responses while the whole purpose of the study was to reveal the role of these responses? Is it because the Ames 35 is so attenuated that it makes other route challenge doses too high?

The Ames strain was reported by R. Lyons to remain fully virulent after the LT deletion, meaning that the Ames 35 virulence should not depend on LT. Why did the authors decide to use this strain to demonstrate the role of LT? Isn't it imperative to obtain a comparative data with the LT deletion mutant to prove the LT relevance and address this issue?

Why was the bacterial load in Fig. 2 measured at 2x10^7 spores within 24 to 32 h? Why is the interval so broad? Did some mice die? Where are the corresponding mortality curves? Based on Fig. 1, at this dose the majority of mice were expected to be dead at the time of sampling, and the results, therefore, would be biased toward survivors.

No competing interests declared.