Skip to main content
. 2015 Jan 12;21(1):134–142. doi: 10.2119/molmed.2014.00189

Figure 4.

Figure 4

Inhibition of cAMP-dependent CFTR channels via JAK3 activation enhances phosphorylated NF-κBp65 nuclear translocation in bronchial cells after exposure to H5N1 HA. Immunofluorescent staining of cultured calu-3 cells was performed following HA addition at two doses for 12 h in the absence or presence of pretreatment with JAK3 inhibitor VI (JAK3inh, 760 nmol/L), forskolin (FSK, 10 μmol/L) or glibenclamide (Gli, 500 μmol/L). (A) The expression of CFTR and translocation of Ser276-phosphorylated NF-κBp65 (p-NF-κB) is shown in calu-3 cells treated with saline; (B) HA alone at 80 μg/mL or (E) 20 μg/mL; (C) HA (80 μg/mL) following pretreatment with either forskolin or (D) JAK3 inhibitor VI; or (F) glibenclamide pretreatment followed by treatment with HA at 20 μg/mL. Scale bars = 40 μm h: high (80 μg/mL), L: low (20 μg/mL). (G) Average fluorescence intensity of CFTR staining is represented. The data are expressed as the mean ± SEM, with n = 3 to 5 per group. *p < 0.05 versus saline control; #p < 0.05 versus the cells with HA (h) treatment alone.