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

Figure 4. The CCL20 promoter region (nucleotides -91 to -50) is critical for the IL-22-attenuated CCL20 expression.

Figure 4

A, Schematic representation of luciferase reporter constructs containing different lengths of the CCL20 promoter. The locations of putative binding sites for various transcription factors are indicated at top. B, Inhibition of H. pylori-induced CCL20 promoter activity by IL-22. 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. Luciferase activity was normalized to the expression of a co-transfected pRL-TK Renilla luciferase plasmid. The activity of each construct is presented as relative luciferase activity of H. pylori-infected cells versus uninfected cells (open bar; set as 1). *, p<0.02; **, p<0.005 for H. pylori + IL-22 versus H. pylori only. Right panel, the inhibitory efficiency (% inhibition) was calculated as follows: [(CCL20 promoter activity in the absence of IL-22 − CCL20 promoter activity in the presence of IL-22) / CCL20 promoter activity in the absence of IL-22]×100. Data represent mean ± SEM from three independent experiments. *, p<0.05 for pGL3-50 versus other reporter constructs.