TNF Receptor 1, IL-1 Receptor, and iNOS Genetic Knockout Mice Are Not Protected from Anthrax Infection

Anthrax produces at least two toxins that cause an intense systemic inflammatory response, edema, shock, and eventually death. The relative contributions of various elements of the immune response to mortality and course of disease progression are poorly understood. We hypothesized that knockout mic...

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Bibliographic Details
Published in:Biochemical and biophysical research communications 2002-03, Vol.292 (1), p.41-44
Main Authors: Kalns, John, Scruggs, Julie, Millenbaugh, Nancy, Vivekananda, Jeeva, Shealy, David, Eggers, Jeffrey, Kiel, Johnathan
Format: Article
Language:English
Subjects:
Animals
anthrax
Anthrax - immunology
Anthrax - prevention & control
Antibodies - pharmacology
Antigens, CD - genetics
Bacillus anthracis
death
IL-1
iNOS
interleukin 1 receptors
knockout
Male
Mice
Mice, Inbred C57BL
Mice, Knockout
mortality
murine
nitric oxide
Nitric Oxide Synthase - genetics
Nitric Oxide Synthase Type II
Receptors, Interleukin-1 - genetics
Receptors, Tumor Necrosis Factor - genetics
Receptors, Tumor Necrosis Factor, Type I
Survival Rate
TNF
TNF-alpha
Tumor Necrosis Factor-alpha - antagonists & inhibitors
Tumor Necrosis Factor-alpha - immunology
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Summary:Anthrax produces at least two toxins that cause an intense systemic inflammatory response, edema, shock, and eventually death. The relative contributions of various elements of the immune response to mortality and course of disease progression are poorly understood. We hypothesized that knockout mice missing components of the immune system will have an altered response to infection. Parent strain mice and knockouts were challenged with LD95 of anthrax spores (5 × 106) administered subcutaneously. Our results show that all genetic knockouts succumbed to anthrax infection at the same frequency as the parent. TNF antibody delayed death but TNF receptor 1 knockout had no effect. IL-1 receptor or iNOS knockouts died sooner. Anthrax was more abundant in the injection site of TNF-α and iNOS knockouts compared to parent suggesting that attenuated cellular response increases rate of disease progression. With the exception of edema and necrosis at the injection site pathological changes in internal organs were not observed.
ISSN:0006-291X
1090-2104
DOI:10.1006/bbrc.2002.6626