Staphylococcal enterotoxin induced IL-5 stimulation as a cofactor in the pathogenesis of atopic disease: the hygiene hypothesis in reverse?

Background: The incidence of Staphylococcus aureus (S. aureus ) colonization on the skin of patients with atopic eczema/dermatitis syndrome (AEDS) is approximately 90% and a variety of evidence implicates epidermal staphylococcal infection as a pathogenic factor in atopic dermatitis. However, the mechanism(s) underlying the effects of this organism in the disease process are unclear. The cellular responses of AEDS suffers and asymptomatic atopic individuals to bacterial superantigens (SAg) were investigated in an attempt to elucidate the role of staphylococcal enterotoxin B (SEB) in atopic disease. Methods: Peripheral blood mononuclear cells (PBMC) were isolated from normal nonatopic adults, asymptomatic atopic individuals, patients with active AEDS and patients with active allergic asthma. The cells were cultured for 24 or 96 h with house dust mite (HDM), SEB and phytohaemagluttinin (PHA), and the supernatants were assayed for cytokine levels. Results: Staphylococcal enterotoxin B selectively stimulates the production of interleukin (IL)-5 in AEDS sufferers but not in asymptomatic atopics or nonatopics. Additionally, we observed comparable susceptibility to the IL-5-stimulatory effects of SEB in allergic asthmatics. Conclusions: Given the central role of IL-5-driven eosinophilia in progression from mild atopy to severe disease, these findings provide a plausible mechanism for the AEDS-promoting effects of staphylococcal SAg. Staphylococcal enterotoxin B may also have a similar role in atopic respiratory disease.