Recently, the other important type of intracellular PRRs, nucleotide-binding oligomerization domain-like receptors (NLRs) has been reported to be strongly associated with inflammatory diseases (5, 6). Particularly, as the best-characterized subtype shown to be expressed in airway, nucleotide-binding domain and leucine-rich repeat protein 3 (NLRP3) inflammasome is considered to be involved in the progress of asthma (7, 8). The NLRP3 inflammasome is a cytosolic protein complex composed of NLRP3, ASC, and pro-caspase-1. The activation of NLRP3 inflammasome proteolytically cleaves pro-caspase-1 into active caspase-1, which in turn promotes maturation of IL-1β and IL-18 (9). And these two NLRP3-associated cytokines are critical in the initiation and amplification of inflammatory process (5). Although NLRP3 inflammasome has been extensively investigated, its role in allergic airway inflammation is still controversial (10–14), and its regulatory networks remain elusive. TLRs and NLRs are two important kinds of PRRs, the formation and activation of NLRP3 inflammasome has been suggested to be initiated by TLRs (8, 15, 16). However, the crosstalk between TLR2 and NLRP3 inflammasome activity in the allergic airway diseases, as well as the underlying mechanism is not clear.