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Updated: Aug 9, 2026
A Mouse Model to Assess Innate Immune Response to Staphylococcus aureus Infection
Published on: February 28, 2019
Action of staphylococcal epidermolytic toxin on mouse skin: an electron microscopic study
Abstract:
The ultrastructure of the skin of 3-day-old mice challenged with small doses of highly purified staphylococcal epidermolytic toxin was examined at various time intervals. Up to 130 min few changes were evident, but at this time wide gaps developed between cells in the horizontal planes of the stratum granulosum, and "bubbles" normally present in the intracellular spece were no longer apparent. Splitting of the desmosomes occurred after the development of distended intercellular spaces. After 20 hr, that is, in the "healing" phase, the appearance suggested that normal maturation of keratinocytes was altered. Also at this time a degree of cell separation was still apparent in the outermost actively maturing layer of the stratum granulosum. The proteinase inhibitor Trasylol was tested for its effect on the toxin when administered up to 45 min after challenge.
Insights
Staphylococcal epidermolytic toxin causes skin cell separation and altered keratinocyte maturation in mice. The proteinase inhibitor Trasylol was tested for its protective effects.
Area of Science:
- Dermatology
- Microbiology
- Toxicology
Background:
- Staphylococcal epidermolytic toxin (ET) is a virulence factor produced by Staphylococcus aureus.
- ET induces skin blistering by targeting desmosomes, crucial for cell adhesion in the epidermis.
Purpose of the Study:
- To investigate the ultrastructural changes in mouse skin following challenge with staphylococcal ET.
- To evaluate the potential protective effect of the proteinase inhibitor Trasylol against ET-induced skin damage.
Main Methods:
- Ultrastructural examination of mouse skin at various time points post-challenge with staphylococcal ET.
- Administration of the proteinase inhibitor Trasylol at different time intervals after toxin challenge.
Main Results:
- Significant intercellular spaces developed in the stratum granulosum by 130 minutes, leading to desmosome splitting.
- Altered keratinocyte maturation and persistent cell separation were observed in the healing phase (20 hours).
- Trasylol was administered up to 45 minutes after toxin challenge to assess its efficacy.
Conclusions:
- Staphylococcal ET rapidly disrupts epidermal cell adhesion and alters keratinocyte maturation.
- Further investigation is warranted to determine the therapeutic potential of Trasylol in mitigating ET-induced skin damage.
