BackgroundAllergic rhinitis (AR) is characterized by airway inflammation in nasal mucosa from inhaled allergens and interleukin (IL)-33 is the potent inducer of Th2 inflammation in allergic nasal epithelium.Staphylococcus epidermidisis one of the most abundant colonizers of the healthy human nasal mucosa and might impact the allergen-induced inflammatory responses in the nasal epithelium. Thus, we sought to characterize the mechanism ofS. epidermidisregulating Th2 inflammation and IL-33 production in AR nasal mucosa.ResultsThe AR symptoms were alleviated and eosinophilic infiltration, serum IgE levels, and Th2 cytokines were significantly decreased in OVA-sensitized AR mice in response to human nasal commensalS. epidermidis. The inoculation ofS. epidermidisto normal human nasal epithelial cells reduced IL-33 and GATA3 transcriptions and also reduced IL-33 and GATA3 expression in AR nasal epithelial (ARNE) cells and the nasal mucosa of AR mice. Our data exhibited that the cellular necroptosis of ARNE cells might be involved in IL-33 production and inoculation ofS. epidermidisdecreased the phosphorylation of necroptosis enzymes in ARNE cells, which was related to the reduction of IL-33 production.ConclusionsWe present that human nasal commensalS. epidermidisreduces allergic inflammation by suppressing IL-33 production in nasal epithelium. Our findings indicate thatS. epidermidisserves a role in blocking allergen-induced cellular necroptosis in allergic nasal epithelium which might be a key mechanism of reduction of IL-33 and Th2 inflammation.Supplementary InformationThe online version contains supplementary material available at 10.1186/s12866-023-02898-7.