In the present study, we found that the levels of BLT1 and BLT2 as well as the synthesis of their ligands LTB4 and 12(S)-HETE were markedly upregulated in our neutrophil-dominant model, and the blockade of BLT1 or BLT2 significantly reduced NLRP3 stimulation and IL-1β synthesis, thus attenuating neutrophilic airway inflammation (Figure 3 and Figure 4). This evidence concerns the gene LTB4R2 and inflammatory response.