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<p>The heteroresistance of <i>Helicobacter pylori</i> to clarithromycin has been investigated intensively. This study aimed to examine the effects of <i>H. pylori</i> strains with heteroresistance to clarithromycin on the apoptosis of gastric epithelial (GES-1) cells. GES-1 cells were infected with clarithromycin-susceptible and -resistant (LSH53S/R) strains isolated from heteroresistant <i>H. pylori</i> LSH53 at a multiplicity of infection of 400:1. Subsequently, the cells were treated with clarithromycin, and apoptosis was assessed via flow cytometry. In addition, western blotting was used to evaluate the expression of apoptosis-related proteins and nuclear factor-kappa B (NF-κB) in GES-1 cells. GES-1 cells were incubated with LSH53S (S<sub>400</sub> group) and LSH53R (R<sub>400</sub> group) strains at an MOI of 400:1 for 24&#xa0;h. The apoptosis of GES-1 cells was higher (<i>P</i> &lt; 0.05) in the S<sub>400</sub> and R<sub>400</sub> groups than in the NC group. The expression of Bcl-2 was lower and that of Bax, the ratio of phosphorylated p65 to total p65 (p-p65/p65) of NF-κB, and cleaved-caspase-3/caspase-3 was higher (<i>P</i> &lt; 0.05) in the S<sub>400</sub> group than in the NC group. Clarithromycin treatment decreased the apoptosis of GES-1 cells infected with the susceptible strain (S<sub>400</sub> + C<sub>2</sub> group) (<i>P</i> &lt; 0.05). In addition, it increased the expression of Bcl-2 and decreased the expression of Bax, p-p65/p65 of NF-κB, and cleaved-caspase-3/caspase-3 in these cells (<i>P</i> &lt; 0.05). Apoptosis and its suppression after clarithromycin treatment were more pronounced in GES-1 cells infected with the susceptible strain than in those infected with the resistant strain of the heteroresistant <i>H. pylori</i>. Mechanistically, <i>H. pylori</i>-mediated apoptosis of GES-1 cells may be associated with the NF-κB/Bcl-2/Bax/caspase-3 pathway.</p>

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Differential apoptosis of GES-1 cells induced by Helicobacter pylori with heteroresistance to clarithromycin

  • 期刊论文

  • 发表日期：

    2026年8月5日

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  • Xue Wang,
  • Yingying Yang,
  • Cui Wang,
  • Lingzhu Gou,
  • Muyang Li,
  • Meirong Feng,
  • Xiaofeng Zhou,
  • Xusheng Ma,
  • Dekui Zhang,
  • Jianwei Yun

摘要

The heteroresistance of Helicobacter pylori to clarithromycin has been investigated intensively. This study aimed to examine the effects of H. pylori strains with heteroresistance to clarithromycin on the apoptosis of gastric epithelial (GES-1) cells. GES-1 cells were infected with clarithromycin-susceptible and -resistant (LSH53S/R) strains isolated from heteroresistant H. pylori LSH53 at a multiplicity of infection of 400:1. Subsequently, the cells were treated with clarithromycin, and apoptosis was assessed via flow cytometry. In addition, western blotting was used to evaluate the expression of apoptosis-related proteins and nuclear factor-kappa B (NF-κB) in GES-1 cells. GES-1 cells were incubated with LSH53S (S400 group) and LSH53R (R400 group) strains at an MOI of 400:1 for 24 h. The apoptosis of GES-1 cells was higher (P < 0.05) in the S400 and R400 groups than in the NC group. The expression of Bcl-2 was lower and that of Bax, the ratio of phosphorylated p65 to total p65 (p-p65/p65) of NF-κB, and cleaved-caspase-3/caspase-3 was higher (P < 0.05) in the S400 group than in the NC group. Clarithromycin treatment decreased the apoptosis of GES-1 cells infected with the susceptible strain (S400 + C2 group) (P < 0.05). In addition, it increased the expression of Bcl-2 and decreased the expression of Bax, p-p65/p65 of NF-κB, and cleaved-caspase-3/caspase-3 in these cells (P < 0.05). Apoptosis and its suppression after clarithromycin treatment were more pronounced in GES-1 cells infected with the susceptible strain than in those infected with the resistant strain of the heteroresistant H. pylori. Mechanistically, H. pylori-mediated apoptosis of GES-1 cells may be associated with the NF-κB/Bcl-2/Bax/caspase-3 pathway.