Fig. 5: IL-1β secretion by LPS and LRZ-stimulated monocytes is differently modulated by drugs interfering with specific cell processes. | Cell Death & Disease

Fig. 5: IL-1β secretion by LPS and LRZ-stimulated monocytes is differently modulated by drugs interfering with specific cell processes.

From: Progressive waves of IL-1β release by primary human monocytes via sequential activation of vesicular and gasdermin D-mediated secretory pathways

Fig. 5

a The cartoon summarizes the targets of the drugs used in these experiments. Bafilomycin (BafA1) blocks the proton influx into endolysosomes, cytocalasin D (cytoD) and latrunculin B (latrB) inhibit actin polymerization. All these drugs induce secretory lysosomes exocytosis8,39,40. 17AAG is an HSP90 inhibitor reported to prevent IL-1β translocation and secretion17. Punicalagin stabilizes lipids in the plasma membrane and inhibit IL-1β secretion in mouse macrophages41. b IL-1β secreted by LPS and LRZ-stimulated monocytes, untreated or treated with BafA1 (BAF), cytocalasin D (CytoD), latrunculin B (Lat), punicalagin (Pun), 17AAG, quantified by ELISA. N = 6. c, d LPS or LPS + 17AAG-treated monocytes were co-stained with anti LAMP2A and anti IL-1β Ab and analyzed by TIRF microscopy (penetration depth 110 nm) after 6 h of incubation (N = 3). (c) Representative LPS and LPS + 17AAG-treated monocytes are shown. Scale bar, 5 μm. d TIRF quantification of the number of LAMP2A+/IL-1β+ vesicles found in monocytes stimulated with LPS or LPS + 17AAG, obtained as in Fig. 4b (N = 3). Data information: In b, d Data are expressed as ng/ml, mean ± SEM. Unpaired t-test was used, and the significance compared with untreated cells is indicated (**P < 0.01, ***P < 0.001)

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