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Updated: Jul 20, 2025

A Mouse Model to Assess Innate Immune Response to Staphylococcus aureus Infection
Published on: February 28, 2019
Staphylococcus xylosus and Staphylococcus aureus as commensals and pathogens on murine skin
Michael Battaglia1, Lee Ann Garrett-Sinha2
1Department of Biochemistry, Jacobs School of Medicine and Biomedical Sciences, State University of New York at Buffalo, Buffalo, NY, 14203, USA.
Abstract:
Skin ulcers, skin dermatitis and skin infections are common phenomena in colonies of laboratory mice and are often found at increased prevalence in certain immunocompromised strains. While in many cases these skin conditions are mild, in other cases they can be severe and lead to animal morbidity. Furthermore, the presence of skin infections and ulcerations can complicate the interpretation of experimental protocols, including those examining immune cell activation. Bacterial species in the genus Staphylococcus are the most common pathogens recovered from skin lesions in mice. In particular, Staphylococcus aureus and Staphylococcus xylosus have both been implicated as pathogens on murine skin. Staphylococcus aureus is a well-known pathogen of human skin, but S. xylosus skin infections in humans have not been described, indicating that there is a species-specific difference in the ability of S. xylosus to serve as a skin pathogen. The aim of this review is to summarize studies that link S. aureus and S. xylosus to skin infections of mice and to describe factors involved in their adherence to tissue and their virulence. We discuss potential differences in mouse and human skin that might underlie the ability of S. xylosus to act as a pathogen on murine skin, but not human skin. Finally, we also describe mouse mutants that have shown increased susceptibility to skin infections with staphylococcal bacteria. These mutants point to pathways that are important in the control of commensal staphylococcal bacteria. The information here may be useful to researchers who are working with mouse strains that are prone to skin infections with staphylococcal bacteria.
Insights
Bacterial skin infections, common in mice, can be severe and impact research. This review details Staphylococcus aureus and xylosus in mouse skin, exploring virulence and host differences.
Area of Science:
- Microbiology
- Immunology
- Dermatology
Background:
- Skin ulcers, dermatitis, and infections are prevalent in laboratory mice, particularly in immunocompromised strains.
- These conditions can range from mild to severe, causing morbidity and complicating experimental data interpretation.
- Staphylococcus species, notably Staphylococcus aureus and Staphylococcus xylosus, are primary bacterial pathogens in murine skin lesions.
Purpose of the Study:
- To review studies on Staphylococcus aureus and Staphylococcus xylosus in mouse skin infections.
- To describe the adherence and virulence factors of these bacteria.
- To explore species-specific differences in pathogenicity between mice and humans, and identify mouse mutants susceptible to staphylococcal skin infections.
Main Methods:
- Literature review of studies on Staphylococcus aureus and Staphylococcus xylosus in mouse skin.
- Analysis of bacterial adherence and virulence factors.
- Comparison of mouse and human skin characteristics relevant to S. xylosus pathogenicity.
- Review of mouse models with increased susceptibility to staphylococcal skin infections.
Main Results:
- Staphylococcus aureus and Staphylococcus xylosus are key pathogens in mouse skin infections.
- Factors influencing bacterial adherence and virulence are crucial for infection development.
- S. xylosus exhibits species-specific pathogenicity, affecting mice but not humans.
- Certain mouse mutants display heightened susceptibility, indicating important host defense pathways.
Conclusions:
- Understanding Staphylococcus species' role in mouse skin infections is vital for research.
- Differences in skin environments may explain S. xylosus's varied pathogenicity.
- Identifying susceptible mouse models aids in studying host-pathogen interactions and immune responses.
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