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. Author manuscript; available in PMC: 2016 Apr 15.
Published in final edited form as: Cancer Res. 2015 Mar 2;75(8):1749–1759. doi: 10.1158/0008-5472.CAN-14-2291

Figure 2. Inactivation of pgdA sensitizes H. pylori to intracellular degradation but not autophagy.

Figure 2

A. Co-cultures of H. pylori and AGS cells were lysed and plated to quantify adherent bacteria. Data represent mean±SEM from at least 3 experiments (NS:Non significant). B. Gentamycin protection assays were performed to quantify viable intracellular H. pylori. (***:p≤0.001). Data represent mean±SEM from at least 3 experiments. C. Transmission electron microscopy of WT strain 7.13 or a pgdA− mutant co-cultured with AGS cells for 4 hours. Arrows: bacteria; arrowheads: phagolysosomal vesicles. D. Confocal images of AGS cells co-cultured with WT 7.13 strain or a pgdA− mutant for 4 hours. Cells were stained with LysoTracker DND-99 (red) and nuclear stain Hoechst 33342 (white). E. Confocal images of AGS cells expressing a GFP-LC3 fusion protein (green) co-cultured with WT strain 7.13 or its pgdA− mutant for 6 hours. Cells were fixed and mounted in media containing DAPI (Blue). F. Western blot of AGS cells co-cultured with WT strain 7.13 or its pgdA− mutant using anti-LC3 and anti-actin antibodies, and subsequent densitometry analysis from three replicates (*:p≤0.05).