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Updated: Aug 22, 2026

Mouse Models Of Helicobacter Infection And Gastric Pathologies
Published on: October 18, 2018
Cellular mucosal defense is attenuated with chronicity of Helicobacter pylori infection
Geoffrey M Matthews1, David Tivey, Adrian G Cummins
1Gastroenterology Department, Women's and Children's Hospital, North Adelaide, South Australia. matthewsg@mail.wch.sa.gov.au
Abstract:
This study assessed the mucosal antioxidant response during acute (mouse) and chronic (adult human) H. pylori infection and following N-acetylcysteine administration. Antral biopsies were obtained from 44 patients (16 infected, 28 noninfected). Sixty-nine mice were sacrificed after 1 (n = 25), 4 (n = 28), or 6 (n = 16) months of infection. A further 29 mice received N-acetylcysteine or water (n = 21) for 14 days following 2.5 weeks of infection. Infected patients showed similar glutathione levels and G6PDH activity to noninfected subjects (P > 0.05). Myeloperoxidase activity was higher in infected patients (P < 0.05). In infected mice, glutathione levels and G6PDH activity were elevated at all time points up 6 months of infection (P < 0.05). Myeloperoxidase activity was increased in infected mice after 1 and 4 months (P < 0.05) but not at 6 months of infection (P > 0.05). N-Acetylcysteine reduced all three parameters in H. pylori-infected mice (P < 0.05). These results suggest an up-regulation of the antioxidant defense system during H. pylori infection in the mouse but not in humans. N-Acetylcysteine reduces the response during infection possibly by lowering the oxidant load.
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