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. 2014 May 13;9(5):e97350. doi: 10.1371/journal.pone.0097350

Figure 5. The NF-κB binding site in the CCL20 promoter is critical for the IL-22-attentuated CCL20 expression.

Figure 5

A, Schematic representation of mutated or deleted CCL20 reporter constructs. Nucleotide substitutions are indicated in lower case and the deleted region is indicated as dash line. B, Inhibitory effects of IL-22 on CCL20 promoter activities. Left panel, AGS cells were co-transfected with the indicated CCL20 promoter constructs and pRL-TK Renilla luciferase plasmid. At 48 h after transfection, cells were infected with H. pylori in the presence or absence of IL-22 and the relative luciferase activity was measured. Data represent the mean ± SEM from three independent experiments. *, p<0.05, **, p<0.005 for H. pylori + IL-22 versus H. pylori only. Right panel, the inhibitory efficiency (% inhibition) were calculated as described in Fig. 4B. *, p<0.05 versus pGL3-862, pGL3/EBPm or pGL3-SPm. C, Inhibitory effects of IL-22 on a promoter containing NF-κB binding sites. AGS cells were co-transfected with pGL4.32 NF-κB luciferase reporter and pRL-TK Renilla luciferase plasmid. At 48 h after transfection, cells were infected with H. pylori in the presence or absence of IL-22 and the relative luciferase activity was measured. Data represent the mean ± SEM from three independent experiments. *, p<0.05 for H. pylori + IL-22 verses H. pylori only.