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. 2021 Mar 3;12(2):395–425. doi: 10.1016/j.jcmgh.2021.02.013

Figure 7.

Figure 7

Rev-erbα in GECs inhibits Reg3b and β-defensin-1 directly, which contributes to H pylori persistence. (A) Primary gastric epithelial cells from uninfected Rev-erbα–/– and WT mice were stimulated with WT H pylori (MOI = 100) for 24 hours. Reg3b and β-defensin-1 production was measured in cell culture supernatants by ELISA (n = 3). (B) In vitro bactericidal assay was performed as described in the Materials and Methods and statistically analyzed (n = 3). (C) AGS cells were cotransfected with β-defensin-1-luc construct or a mutant construct and Rev-erbα-pcDNA3.1 or pcDNA3.1 (control vector) for 48 hours. Luciferase activity was measured to assess β-defensin-1 promoter activity (n = 3). (D) Representative data and statistical analysis of chromatin immunoprecipitation assay in AGS cells infected with WT H pylori or ΔcagA, followed by regular PCR with primers designed for Rev-erbα binding site of β-defensin-1 promoter region (n = 3). ∗∗P < .01, n.s. P > .05 for groups connected by horizontal lines.