Long-term stress and Helicobacter pylori infection independently induce gastric mucosal lesions in C57BL/6 mice.
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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ABSTRACT: There is a large literature showing that unemployment has a negative effect on mental health, but little evidence exists on how mental illness affects the unemployeds’ chances of re-employment or the risk of labour market exit. We study how purchase of pharmaceutical products for severe mental illnesses during unemployment affects re- employment and labour market exit probabilities. Within the framework of a multivariate duration model we apply the ‘timing-of-events’ method, which explicitly makes use of the information that pharmaceutical treatment can begin at different points of time during an unemployment spell. In the absence of instrumental variables this method allows for causal inference in presence of unobserved heterogeneity, but at the cost of strong assumptions. The basis for our analysis is state-of-the-art register-based data, which gives insight on the timing, type, and volume of drug purchase as well as labour market histories for a random sample of the Danish population. We find a significant and strong negative effect of periods with drug treatment on the employment chances. During the treatment with drugs, the job-finding rate is reduced substantially relative to what it would have been in absence of a drug treated mental illness. Importantly, our results not only show that drug treated mental illness prolongs the unemployment duration, but it also increases the labour market exit rate.SSRN Electronic Journal 07/2010; DOI:10.2139/ssrn.1672026
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ABSTRACT: Helicobacter pylori infection is a risk factor for development of peptic ulcers, and psychological stress (PS) may have a role in the pathogenesis of this condition. However, no interaction between PS and H. pylori infection (HI) has been established in the development of peptic ulcer, because colonization by H. pylori is the first step in the infection of the gastric mucosa, we examined H. pylori colonization of the stomach in BALB/c mice after PS. The mice were subjected to PS in a communication box test, in which they observed other mice experiencing a physical stressor (electrical) before they were inoculated with H. pylori. We found that the H. pylori colonization in the stomach of psychologically stressed mice was significantly greater than in the control mice (P < 0.05), and histological examination showed that the gastric mucosal injury in the stressed mice was more extensive than in the control mice (P < 0.05). To explore the underlying mechanisms, we administered RU486 (a type II glucocorticoid (GC) receptor antagonist) to antagonize the effect of endogenous corticosterone: this treatment decreased colonization by H. pylori in the psychologically stressed mice. We conclude that HI of the stomach of BALB/c mice is enhanced by PS, and the effect may be mediated by GCs.Stress (Amsterdam, Netherlands) 11/2009; 12(6):478-85. DOI:10.3109/10253890802642188 · 3.46 Impact Factor