The internalization of Helicobacter pylori plays a role in the failure of H. pylori eradication

Background Helicobacter pylori (H. pylori) internalization involves invasion of cells by the bacterium. Several studies have shown that H. pylori can invade human gastric epithelial cells, immune cells, and Candida yeast in vivo and in vitro. Whether bacterial invasion plays a role in eradication failure is unclear. Aim To investigate the relationship between H. pylori invasion of GES‐1 cells and H. pylori eradication failure. Materials and Methods Forty‐two clinical strains isolated from H. pylori‐positive patients with different outcomes after treatment with furazolidone‐based therapy were examined (17 failures and 25 successes). The H. pylori strains were shown to be susceptible to amoxicillin and furazolidone, and the patients also exhibited good compliance. Genotyping was performed for cagA and vacA (s and m). The antibiotic susceptibility of the strains to amoxicillin, furazolidone, clarithromycin, metronidazole, and levofloxacin was determined by E‐tests. The levels of H. pylori invasion of GES‐1 cells were detected by gentamicin colony‐forming unit assays. Results The internalization level in the eradication success group was 5.40±5.78 × 10−3 cfu/cell, and the median was 6.194 × 10−3 cfu/cell; the internalization level in the eradication failure group was 8.98±5.40 × 10−3 cfu/cell, and the median was 10.28 × 10−3 cfu/cell. The eradication failure group showed a greater invasion level than the eradication success group (P.05). Conclusions The results showed that H. pylori invasion of the gastric epithelia might play a role in eradication failure.