Fig. 3 | Scientific Reports

Fig. 3

From: Helicobacter pylori CagA mediated mitophagy to attenuate the NLRP3 inflammasome activation and enhance the survival of infected cells

Fig. 3

H. pylori CagA induces mitophagy in infected gastric epithelial cells. GES-1 and AGS cells infected with H. pylori for 48 h at an MOI of 60, respectively. (A) The expression of mitophagy- related proteins PINK1, PARKIN, P62, LC3, VDAC1and TOM20 were detected by western blotting. The membrane strips were cut before hybridization with antibodies, which resulted in the inability to provide the original full-length blot images.; (B) The immunofluorescence signal accumulation of LC3 co-localization with mitochondria were observed by confocal microscopy, Scale bar: 10 μm; (C) The accumulation of autophagosomes and autolysosomes was performed by TEM, Scale bar: 5 μm and 1 μm. The figure presents the average of three independent experiments. Data are presented as the means ± SD. Error bars represent the standard deviation. control, the uninfected cells; GZ7/ΔcagA, the GZ7/ΔcagA strains infected cells; GZ7/cagA, the GZ7/cagA strains infected cells; *p < 0.05, **p < 0.01; GZ7/cagA vs control, GZ7/cagA vs GZ7/ΔcagA.

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