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. 2021 Jan 6;12(1):49. doi: 10.1038/s41419-020-03335-7

Fig. 2. Gefitinib promotes IL-1β release by stimulating the NLRP3 inflammasome.

Fig. 2

A The inhibitory effect of KCl on gefitinib-induced IL-1β release. PMA-differentiated THP-1 cells were treated with 20 μM gefitinib for 8 h in the presence of the indicated concentrations of KCl. Cell-free supernatants (Sup) and cell lysates were subjected to immunoblotting with the indicated antibodies. B The inhibitory effect of glyburide on gefitinib-induced IL-1β release. PMA-differentiated THP-1 cells were pretreated with 100 μM glyburide for 0.5 h and then treated with 20 μM gefitinib for 8 h or 200 µg/ml Alum for 6 h. Cell-free supernatants (Sup) and cell lysates were subjected to immunoblotting with the indicated antibodies. C, D, E Requirement of the NLRP3 inflammasome for gefitinib-induced IL-1β release. PMA-differentiated WT, NLRP3 KO, ASC KO, and caspase-1 KO THP-1 cells were treated with 20 μM gefitinib for 8 h. Cell-free supernatants (Sup) and cell lysates were subjected to immunoblotting with the indicated antibodies. F ASC oligomerisation assay in NLRP3 KO THP-1 cells. PMA-differentiated WT and NLRP3 KO THP-1 cells were treated with 20 μM gefitinib for 8 h. DSS-mediated crosslinked pellets (crosslinked-pellet) and soluble lysates (Input) were subjected to immunoblotting with the indicated antibodies. All data in Fig. 2 are representatives of at least five independent experiments.