Staphylococcal Enterotoxin Gene B Relevant to Atopic Dermatitis Alters the Expression of Kallikreins and β-defensin 2 in HaCaT Cells

Atopic dermatitis (AD) is a chronic, recurrent inflammatory skin disorder characterized by abnormal skin barrier function, immune inflammation, and disrupted skin microbiome. The dynamic alterations of staphylococcus aureus ( S . aureus) superantigens, kallikreins (KLKs), and β-defensin 2 (β-HBD2) in keratinocytes play pivotal roles in the pathogenesis of AD. However, the mechanisms of their action remain poorly understood. In our study, we utilized staphylococcal enterotoxin gene B (SEB) to stimulate HaCaT cells. Although SEB did not significantly alter the proliferation of HaCaT cells nor increase cell apoptosis, KLKs were increased and β-HBD2 was decreased to varying degrees, indicating that KLKs activation and β-HBD2 reduction may facilitate the induction of AD and the colonization of S. aureus. Our investigation into the in vitro cellular mechanisms of SEB on AD progression provides a theoretical foundation for future AD therapies.