Figure 2.

Autophagy is down-regulated in human gastric mucosa of patients infected with CagA positive H. pylori strains. (A) Immunohistochemistry showing SQSTM1 expression in the gastric mucosa of patients without H. pylori infection and those infected with cagA⁻/vacA^s1m2 or cagA⁺/vacA^s1m2 strains of H. pylori. The intensity of staining is shown in the right graph and the data are expressed as mean ± SEM. (B) Western blot assay showing the protein levels of MAP1LC3B-II, SQSTM1 and LAMP1 in the gastric mucosa of patients of normal control (patients 1–4), cagA⁻/vacA^s1m2(patients 5–8), and cagA⁺/vacA^s1m2 (patients 9–12) with the rates to β-actin being illustrated in the graphs in which the data are expressed as mean ± SEM. (C) Transmission electron microscopy showing autophagosomes in gastric biopsy sections of patients without H. pylori infection and those infected with cagA⁻/vacA^s1m2 or cagA⁺/vacA^s1m2 strains of H. pylori. Normal controls are patients without H. pylori infection. The white arrows indicate the autophagosomes. The numbers of autophagic vacuoles per cell in each TEM section (n = 35 cells) are shown in the right graph and the data are expressed as mean ± SEM. Experiments performed in triplicate showed consistent results. ^*P < 0.05, or ^**P < 0.01.