Figure 1.

H. pylori infection affects DNA damage response signaling pathway. (a) Representative images of Western blot analysis for γH2AX in GES-1 cells with H. pylori NCTC11637 infection at different MOI or at different time points. (b) The comet assay for assessing DNA damage in GES-1 cells with or without H. pylori. Scale bar, 10 μm. (c) Immunochemistry for γH2AX in gastric tissues collected from Mongolian gerbils that were challenged with H. pylori NCTC11637 strain or Brucella broth for 6 months (H. pylori, n = 30; control, n = 15) or 12 months (H. pylori, n = 30; control, n = 10). (d) Representative images (200× magnification) of Western blot analysis for p-p53 (Ser20), p-p53 (Ser15), p-Chk2 (Thr168), Chk1, p-ATM (Ser1981), ATM in GES-1 cells infected with H. pylori NCTC11637 at different time points. (e) Flow cytometry analysis for cell cycle distribution after H. pylori infection. (f) Representative immunohistochemical staining for p-ATM (S1981), p-Chk2 (T68) and p-p53 (S15) in a series of human gastric tissues with Correa cascade from CNAG, IM, Dys and GC. Quantitative analysis of the immunohistochemical staining results in gastric tissues. *P < .05, **P < .01. (g) Representative images of Western blot analysis for Rad51 in GES-1 cells with H. pylori NCTC11637 infection. (h) Representative images of Western blot analysis for γH2AX, p-p53 (Ser20) and p-p53 (Ser15) in GES-1 cells, which were treated with H. pylori in combination with plasmid expressing Rad51 or Rad51 siRNAs. A representative blot of three independent experiments was shown. (i) After transfected with Rad51 expression plasmid or Rad51 siRNAs, the comet assay was performed to detect DNA damage and the length of tail DNA was evaluated in gastric cells with H. pylori infection. (j) Immunohistochemistry staining images (200× magnification) for Rad51 in gastric tissues of Mongolian gerbils infected with H. pylori. Scale bar: 50 μm. All in vitro experiments were independently repeated three or more times. *P < .05, **P < .01.