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An experimental model of cutaneous infection induced by superantigen-producing Staphylococcus aureus
1Departments of Dermatology and Rheumatology, Sahlgrenska University Hospital, Göteborg, Sweden. lena.molne@immuno.gu.se
Abstract:
Skin infections caused by Staphylococcus aureus, such as erysipelas, are commonly occurring, painful, and costly for society. Despite the high prevalence of this condition, little is known about the host immune responsiveness and bacterial virulence factors during S. aureus dermatitis. We present here a mouse model of infectious dermatitis in which S. aureus is inoculated by an intracutaneous injection to the shaved back of NMRI mice. Visible skin inflammation, characterized by redness and swelling, was noted 48 h after inoculation of staphylococci in mice that received 2 x 108 colony-forming units of S. aureus. Microscopic evaluation revealed a dermal and subcutaneous infiltrate rich in macrophages and neutrophilic granulocytes already within 6 h after inoculation. A sparse influx of T lymphocytes was noted somewhat later. Bacterial cultures from skin revealed high numbers of staphylococci early after inoculation, with a successive decline during 2 wk follow-up. Total white blood cell count as well as the number of polymorphonuclear leukocytes peaked 2 d after bacterial inoculation. Also, serum interleukin-6 levels peaked within 2 d, with a 10-fold increase compared to non-infected control mice, indicating a systemic reaction to skin infection. The role of toxic shock syndrome toxin 1 in the pathogenesis of the dermatitis was assessed using isogenic S. aureus strains. Even though the gross inflammatory skin reaction was similar for mice infected with either of the strains, it was apparent that bacteria secreting toxic shock syndrome toxin 1 preferentially triggered influx of T lymphocytes to the skin. In addition, mice inoculated with staphylococci producing toxic shock syndrome toxin 1 showed a weight decrease during the experiment whereas mice inoculated with the isogenic strain showed a weight increase. This model of staphylococcal dermatitis will enable future in-depth studies regarding the host-bacterium relationship.
Insights
This study introduces a new mouse model for Staphylococcus aureus skin infections, revealing key immune responses and the impact of toxic shock syndrome toxin 1 on T lymphocyte influx and weight loss.
Area of Science:
- Immunology
- Microbiology
- Dermatology
Background:
- Staphylococcus aureus skin infections, like erysipelas, are prevalent and costly.
- Understanding host immune responses and bacterial virulence factors in S. aureus dermatitis is limited.
Purpose of the Study:
- To establish a mouse model for infectious dermatitis caused by S. aureus.
- To investigate host immune responses and the role of toxic shock syndrome toxin 1 (TSST-1) in S. aureus-induced skin inflammation.
Main Methods:
- Intracutaneous inoculation of S. aureus into NMRI mice.
- Monitoring of visible skin inflammation, histopathological analysis, bacterial load assessment, and systemic immune markers (white blood cell count, IL-6).
- Utilizing isogenic S. aureus strains to assess the role of TSST-1.
Main Results:
- Visible skin inflammation (redness, swelling) appeared 48 hours post-inoculation.
- Early dermal infiltrate of macrophages and neutrophils, followed by T lymphocytes.
- S. aureus bacterial load decreased over 2 weeks; systemic immune response indicated by elevated IL-6 and white blood cell counts.
- TSST-1 secreting strains induced greater T lymphocyte influx and caused weight loss in mice.
Conclusions:
- The developed mouse model effectively replicates S. aureus infectious dermatitis.
- TSST-1 plays a significant role in modulating the host immune response, particularly T lymphocyte recruitment, and impacts host physiology.
- This model facilitates further research into host-pathogen interactions in staphylococcal skin infections.