Finally, consistent with the downregu-lation of TLR2/MyD88/NF-κB pathway proteins following treatment with BML-111- and anti-IL-1β antibodies, the OVA-induced airway inflammation was restrained, as shown by the reduced serum levels of IL-1β, IL-4 and IL-8, as well as BALF levels of IL-1β, IL-4, IL-8, OVA-IgE, and leukocyte counts; furthermore, peribronchial inflammation of lungs induced by OVA was ameliorated by BML-111- and anti-IL-1β antibodies. The gene discussed is IL4; the disease is inflammatory response.