<i>H. pylori</i> strains down-regulate Cav1 gene expression <i>in vitro</i> and <i>in vivo</i> independently of CagA.

<p>(A) Reduced expression of mouse C<i>av1</i> mRNA after an 11-month infection with CagA-delivery defective <i>H. pylori</i> strain SS1. CT-values from RT-qPCRs on total RNA extracted from resected stomachs were normalized to b2M and presented as mean ± S.E. (n = 15 per group); *p = 0.0081 KO <i>versus</i> WT. (B–C) CagA-proficient G27 and CagA-delivery incompetent SS1 <i>H. pylori</i> strains both down-regulate Cav1 mRNA and protein expression in human GC cell lines independently of CagA. MDCK, N87 and MKN45 cells were infected with the respective <i>H. pylori</i> strain (MOI = 100) for the indicated times. Left: CT-values from RT-qPCRs on total RNA (3 days upon infection) were normalized to b2M and calculated as % ± S.E. (n = 3 per cell lines); (B) *p = 0.0043 (MDCK), 0.0001 (N87) and 0.0345 (MKN45), (C) *p<0.05 for all three cell lines; <i>H. pylori versus</i> mock. Right: Representative WBs are shown. (D) <i>H. pylori</i> inhibits Cav1 promoter activity. HEK293 and MKN45 cells were transiently transfected for 24 h with pGL3-<i>CAV1</i>p, SeRE or BSEP firefly luciferase reporter plasmids together with renilla control plasmid, followed by infection with <i>H. pylori</i> G27 (MOI = 100) for additional 16 h. Firefly luciferase activity was normalized to renilla and is presented as % ± S.E. (n = 3); *p = 0.002 (Cav1) for HEK293, 2.7×10⁻⁶ (Cav1) and 0.0052 (SeRE) for MKN45, <i>H. pylori versus</i> mock.