Long-term stress and Helicobacter pylori infection independently induce gastric mucosal lesions in C57BL/6 mice.

Dept. of Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea.
Scandinavian Journal of Gastroenterology (Impact Factor: 2.33). 12/2002; 37(11):1259-64. DOI: 10.1080/003655202761020515
Source: PubMed

ABSTRACT Long-term psychological stresses may have a role in the pathogenesis of peptic ulcer. However, the interaction between stress and Helicobacter pylori infection in the development of peptic ulcer is not established. The aim of this study was to elucidate the roles of long-term stress and H. pylori infection in the development of gastric mucosal lesions in mice.
The Sydney strain (SS1) of H. pylori was inoculated into the stomach of C57BL/J6 mice. Twelve weeks later, mice with or without H. pylori infection were exposed to long-term repeated water-immersion-restraint stress (WIRS) for 12 h per day, 3 times per week, for 8 weeks. Gastric mucosal lesions were evaluated both macroscopically (ulcer index) and microscopically (Updated Sydney System).
The long-term WIRS induced mild inflammation, oedema, interstitial haemorrhage and superficial erosions in the stomach of mice both with and without H. pylori infection. The degree of mucosal inflammation or atrophy in H. pylori-infected mice was not influenced by the stress. In the mice without H. pylori infection, the ulcer index of the stressed mice was greater than that of non-stressed mice (1.66 +/- 0.39 versus 0.17 +/- 0.08, P = 0.007). In the mice with H. pylori infection, the ulcer index (mean +/- s(x)) of the stressed mice was also greater than that of non-stressed mice (2.31 +/- 0.59 versus 0.64 +/- 0.22, P = 0.027).
The present study showed that long-term stress can induce gastric mucosal inflammation and erosions, and this effect may occur independently of H. pylori infection.

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