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. 2017 Sep 5;32(1):155–167. doi: 10.1096/fj.201700114RRR

Figure 6.

Figure 6.

Basolateral PAR-2 stimulation increases CBF in primary human sinonasal ALIs. A) β-tubulin IV staining of cilia in primary human ALI cultures. B) 2FLI (18 or 1.8 μM) increased CBF (normalized to initial CBF at time 0 (CFBt = 0). C) Trypsin, but not AY-NH2, increased CBF. Trace shows averages of 3 experiments each from 3 individuals (patients with CRS, ethmoid sinus-derived ALIs). D, E) 2FLI-activated increases in CBF were blocked by Ca2+ chelation (BAPTA-preloading and extracellular EGTA; D) but not by abolishment of NO signaling (l-NAME pretreatment. E) Traces show average of 3 experiments each from 3 individuals (patients with CRS, ethmoid sinus-derived ALIs). F) Peak CBF/CBFt = 0 values (n = 4–5 experiments from 4 to 5 patients each; 1 ALI per patient). G) Graphs show peak CBF values in response to 2FLI from ALIs from 3 separate turbinate samples compared with 3 separate ethmoid samples and 3 separate control patients compared with 3 separate patients with CRS. H) 2FLI (1.8 and 18 µM) increased CBF in primary bronchial ALI cultures. Trace shown is the average of 4 ALI cultures (2 donors; 2 ALIs each). NHBE, human bronchial epithelial cells. I) Peak CBF increases to apical and basolateral 2FLI. N.s., not signficant. *P < 0.05, **P < 0.01.