An experimental model of cutaneous infection induced by superantigen-producing Staphylococcus aureus.
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.
Mölne
L
L
Departments of Dermatology and Rheumatology, Sahlgrenska University Hospital, Göteborg, Sweden. lena.molne@immuno.gu.se
Tarkowski
A
A
D000818:Animals; D001402:B-Lymphocytes / Q000276:immunology; D015496:CD4-Positive T-Lymphocytes / Q000737:chemistry; D018414:CD8-Positive T-Lymphocytes / Q000737:chemistry; D003872:Dermatitis / Q000188:drug therapy / Q000382:microbiology*; D004195:Disease Models, Animal; D007074:Immunoglobulin G / Q000097:blood; D007075:Immunoglobulin M / Q000097:blood; D007150:Immunohistochemistry; D015850:Interleukin-6 / Q000097:blood; D016177:Macrophage-1 Antigen / Q000032:analysis; D008297:Male; D051379:Mice; D008815:Mice, Inbred Strains; D013203:Staphylococcal Infections; D013211:Staphylococcus aureus / Q000276:immunology*; D018089:Superantigens; D013601:T-Lymphocytes / Q000276:immunology
D007074:Immunoglobulin G; D007075:Immunoglobulin M; D015850:Interleukin-6; D016177:Macrophage-1 Antigen; D018089:Superantigens