However, the mechanism underlying TLR2 mediation of allergic airway inflammation is still unknown. NLRP3 inflammasome is one of the most extensively characterized NLRs due to its relevance in human inflammatory disorders such as asthma. Invading pathogens including viral or bacterial which commonly associated with asthma exacerbation, have been shown to trigger NLRP3 activation (5, 41). IL-1β is increased in the serum and BALF of human asthmatics, and administration of IL-1β induces airway hyper-reactivity (12, 13). Increased expressions of NLRP3, caspase-1 and IL-1β are found in macrophages as well as neutrophils in sputum of neutrophilic asthma (14). Consistent with these studies, our present study showed that in WT mice, OVA challenge substantially increased protein expression of NLRP3, mature IL-1β and caspase 1(p20) in lung tissues, markedly elevated the levels of NLRP3-associated IL-1β and IL-18 in BALF. However, this effect was only seen in WT mice, but not in TLR2−/− mice. The interaction between TLR2 and NLRP3 inflammasome has been also reported in various cell types. In monocytes (42), macrophages (43, 44), bone marrow-derived DCs (45) and several different cell lines (46, 47), lacking TLR2 failed to upregulate NLRP3 inflammasome as well as its substrate IL-1β. Therefore, our results have suggested that activation of NLRP3 inflammasome induced by OVA requires TLR2 signaling, thus TLR2 may mediate allergic airway inflammation through regulating NLRP3 inflammasome activity.