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. Author manuscript; available in PMC: 2016 Jun 1.
Published in final edited form as: Pediatr Res. 2015 Sep 2;78(6):650–656. doi: 10.1038/pr.2015.168

Figure 1.

Figure 1

Fluticasone inhibits TNF-α-induced CXCL10, CXCL8, and CCL5 production by fetal human airway smooth muscle (ASM) cells. Quiescent fetal ASM cells generated small amounts of CXCL10 (Δ), CXCL8 (X), and CCL5 (□), protein (panel a). Stimulation with TNF-α resulted in a dose-dependent increase in production of all three cytokines. Fluticasone (FP) attenuated TNF-α (20 ng/ml) stimulated production of CXCL10, CXCL8, and CCL5 by 50, 25, and 85% respectively (panels b–d). Note fetal ASM cells were treated with vehicle or TNF-α following pretreatment (1 h) with vehicle or fluticasone. Supernatant chemokine concentrations were determined by enzyme-linked immunosorbent assay as described in the Methods section and expressed in picograms per milliliter ± SEM of three separate experiments, *P < 0.05, **P < 0.01.