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A Reproducible Intensive Care Unit-Oriented Endotoxin Model in Rats
Published on: February 20, 2021
Murine models of staphylococcal enterotoxin B-induced toxic shock
Teresa Krakauer1, Marilyn Buckley, Diana Fisher
1Integrated Toxicology Division, U.S. Army Medical Research Institute of Infectious Diseases, Fort Detrick, MD 21702-5011, USA.
Abstract:
Staphylococcal enterotoxin B (SEB) is a member of a large family of structurally related exotoxins produced by Staphylococcus aureus, which is the etiological agent responsible for toxic shock and staphylococcal food poisoning. SEB binds directly to the major histocompatibility complex (MHC) class II molecules on antigen-presenting cells and T-cell receptors on T cells triggering T-cell proliferation and mediator release. SEB is a biothreat agent because of its ability to potently activate cells of the immune system. In vivo animal models are critical in the development of therapeutics against SEB-induced shock. Our results show that three different mouse strains with different susceptibility to SEB can be used to study SEB-induced shock without the use of potentiating agents. The hypothermic response, weight loss, and induction of serum monocyte chemoattractant protein 1 (MCP-1), interleukin 2 (IL-2), and IL-6 correlated with mortality in all three models.
Insights
Staphylococcal enterotoxin B (SEB) is a biothreat agent. This study shows that three mouse models can effectively study SEB-induced shock, correlating immune responses with mortality.
Area of Science:
- Immunology
- Microbiology
- Toxicology
Background:
- Staphylococcal enterotoxin B (SEB) is an exotoxin from Staphylococcus aureus, causing toxic shock and food poisoning.
- SEB interacts with MHC class II and T-cell receptors, activating immune cells and releasing mediators.
- SEB is recognized as a biothreat agent due to its potent immune system activation.
Purpose of the Study:
- To evaluate in vivo animal models for studying SEB-induced shock.
- To identify reliable indicators of SEB toxicity and mortality in different mouse strains.
Main Methods:
- Utilized three mouse strains with varying susceptibility to SEB.
- Monitored hypothermic response, weight loss, and serum levels of MCP-1, IL-2, and IL-6.
- Correlated these parameters with mortality rates.
Main Results:
- All three mouse strains demonstrated SEB-induced shock without needing potentiating agents.
- Hypothermia, weight loss, and elevated MCP-1, IL-2, and IL-6 levels correlated with mortality across models.
- These findings establish viable animal models for SEB research.
Conclusions:
- Three distinct mouse strains are suitable for studying SEB-induced shock.
- Key physiological and immunological markers predict SEB toxicity and mortality.
- These models facilitate the development of countermeasures against SEB biothreats.
