Staphylococcus aureus colonization in contact hypersensitivity induces a shift in cutaneous cytokine milieu from a Th1- to a Th2-type profile

• Main Authors: Masumi Ueda, Fusako Okazaki, Hiroko Kanzaki, Joji Tada, Jirô Arata
• Format: Article
• Language: English
• Published: Elsevier 2003-01-01
• Series: Allergology International
• Subjects: atopic dermatitis; Staphylococcus aureus; Th1 cells; Th2 cells
• Online Access: http://www.sciencedirect.com/science/article/pii/S1323893015311667

Background: Colonization of atopic dermatitis lesions with Staphylococcus aureus is a frequent phenomenon and may exacerbate inflammation of the skin. The aim of the present study was to determine the effect of S. aureus on T cell-mediated immune responses in contact hypersensitivity caused by a hapten or a protein with large molecule. Methods: Staphylococcus aureus or phosphate-buffered saline was inoculated on experimental contact dermatitis induced by 2,4,6-trinitro-1-chlorobenzene (TNCB) or house dust mite antigen. At various times after inoculation, the experimental lesions were examined histologically and immunohistochemically. Furthermore, the kinetics of cytokine patterns (interferon (IFN)-γ, interleukin (IL)-2, IL-4 and IL-5) in each lesion were analyzed by reverse transcription-polymerase chain reaction. Results: In TNCB-challenged lesions inoculated with S. aureus, the levels of IL-2 mRNA decreased; in contrast, mRNA levels of IL-4 and IL-5 were upregulated. In mite antigen-challenged lesions, IL-4 and IL-5 mRNA expression was detected throughout the period of the investigation, even without S. aureus inoculation. Interferon-γ mRNA expression in mite dermatitis without S. aureus inoculation was observed only in the later period and IL-2 mRNA expression in mite dermatitis with S. aureus was suppressed and observed much later than in the control group. Conclusions: Infestation of S. aureus on skin lesions in experimental contact hypersensitivity induces a shift in the immune reaction from a Th1- to a Th2-dominant response.