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Cellular mucosal defense is attenuated with chronicity of Helicobacter pylori infection.

Geoffrey M Matthews, David Tivey, Adrian G Cummins, Ross N Butler
Other Digestive diseases and sciences 2004 4 sitasi
PubMed DOI
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Study Design

Jenis Studi
Observational Study
Ukuran Sampel
44
Populasi
44 adult patients (16 H.pylori+) and 69 mice
Intervensi
Cellular mucosal defense is attenuated with chronicity of Helicobacter pylori infection. N-acetylcysteine (in mouse experiments)
Pembanding
H. pylori-infected vs uninfected
Luaran Utama
Mucosal antioxidant response
Arah Efek
Negative
Risiko Bias
Moderate

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.

TL;DR

Results suggest an up-regulation of the antioxidant defense system during H. pylori infection in the mouse but not in humans and N-Acetylcysteine reduces the response during infection possibly by lowering the oxidant load.

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