BACKGROUND: Despite Helicobacter pylori eradication, gastric inflammation persists for months or years. Preliminary results have indicated that an increase in gastric permeability could be one reason. Our aim was to evaluate the effect of a mucosal protective drug, rebamipide, on gastric permeability in a model of H. felis-infected mice. METHODS: Thirty-three C57/BL6 mice were inoculated with H. felis, and seven controls were kept non-inoculated. After 2 months 20 infected mice were treated with omeprazole, amoxicillin, and clarithromycin for 1 week and then for 4 weeks with either rebamipide (n = 9) or placebo (n = 11). The 13 remaining mice were kept untreated. After cessation of treatment, a fragment of antrum obtained from each mouse was mounted in a small Ussing chamber to study the electric resistance of the tissue (R) and antral permeability. RESULTS: No modification of the paracellular permeability (R, JNa, JMan) was observed in either group. However, the transcellular permeability to horseradish peroxidase (HRP) was significantly increased in H. felis-infected non-treated mice (1131 +/- 463, 948 +/- 339, and 182 +/- 312 ng/h x cm2) as compared with non-infected controls (469 +/- 262, 458 +/- 261, and 10 +/- 6 ng/ h x cm2, for J3H-HRP, JD, and JHRPi, respectively) (P < 0.003). Eradication of the bacteria by antibiotics without subsequent treatment with rebamipide led to a non-significant decrease in the HRP fluxes. However, when rebamipide was used after the antibiotic treatment, a significant (P < 0.01) decrease in HRP fluxes as compared with non-treated mice was observed. CONCLUSIONS: These results confirm that gastric permeability to macromolecules remains increased despite H. felis eradication and show that rebamipide can facilitate the normalization of gastric permeability to macromolecules after bacterial eradication.
BACKGROUND: Despite Helicobacter pylori eradication, gastric inflammation persists for months or years. Preliminary results have indicated that an increase in gastric permeability could be one reason. Our aim was to evaluate the effect of a mucosal protective drug, rebamipide, on gastric permeability in a model of H. felis-infected mice. METHODS: Thirty-three C57/BL6 mice were inoculated with H. felis, and seven controls were kept non-inoculated. After 2 months 20 infected mice were treated with omeprazole, amoxicillin, and clarithromycin for 1 week and then for 4 weeks with either rebamipide (n = 9) or placebo (n = 11). The 13 remaining mice were kept untreated. After cessation of treatment, a fragment of antrum obtained from each mouse was mounted in a small Ussing chamber to study the electric resistance of the tissue (R) and antral permeability. RESULTS: No modification of the paracellular permeability (R, JNa, JMan) was observed in either group. However, the transcellular permeability to horseradish peroxidase (HRP) was significantly increased in H. felis-infected non-treated mice (1131 +/- 463, 948 +/- 339, and 182 +/- 312 ng/h x cm2) as compared with non-infected controls (469 +/- 262, 458 +/- 261, and 10 +/- 6 ng/ h x cm2, for J3H-HRP, JD, and JHRPi, respectively) (P < 0.003). Eradication of the bacteria by antibiotics without subsequent treatment with rebamipide led to a non-significant decrease in the HRP fluxes. However, when rebamipide was used after the antibiotic treatment, a significant (P < 0.01) decrease in HRP fluxes as compared with non-treated mice was observed. CONCLUSIONS: These results confirm that gastric permeability to macromolecules remains increased despite H. felis eradication and show that rebamipide can facilitate the normalization of gastric permeability to macromolecules after bacterial eradication.