Disruption of CFTR activity does not increase IL-1β production in PBMCs and THP-1 cells
A previous study has indicated a role for chloride ion concentration in suppression of NLRP3 inflammasome activation [34]. To determine whether CFTR dysfunction alters IL-1β production, THP-1 cells and PBMCs from CF patients and healthy controls were treated with the CFTR inhibitor, CFTRinh172, prior to simulation with live P. aeruginosa. Treatment with CFTRinh172 did not alter IL-1β or IL-8 production in control subjects or CF patients (Fig. 8a–b). Similarly, IL-1β production was not different in monocyte-derived macrophages or THP-1 reporter cells treated with CFTRinh172 (Fig. 8c–d). IL-8 (Fig. 8e) and NF-κB activity (Fig. 8f) were also unchanged in CFTRinh172-treated THP-1 reporter cells.
10.1371/journal.pone.0037689.g008 Figure 8  Disruption of CFTR activity does not increase IL-1β production in PBMCs or macrophages.
PBMCs from CF patients (n = 15) and controls (n = 13) were treated with CFTRinh172 (10 µM) for 18 hours prior to stimulation with live PAO1 (MOI = 1). (A) IL-1β and (B) IL-8 production was measured at 24 hours. (C) Monocytes from controls (n = 3) were differentiated into macrophages. Macrophages were treated with CFTRinh172, stimulated as per monocytes, and measured for IL-1β production at 24 hours. THP-1 reporter cells were treated with CFTRinh172 24 hours prior to stimulation with PAO1 and measured for (D) IL-1β secretion, (E) IL-8, and (F) NF-κB/AP-1 activity at 24 hours (n = 4).

D