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.
"A study of peptic ulcer patients in a Thai hospital showed that chronic stress was strongly associated with an increased risk of peptic ulcer, and a combination of chronic stress and irregular mealtimes was a significant risk factor (Wachirawat et al., 2003). Another study on mice has shown that both long-term water-immersion-restraint stress and helicobacter pylori infection were independently associated with the development of peptic ulcers (Kim et al., 2002). "
[Show abstract][Hide abstract] 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.
"Duodenal ulcer is a mucosal erosion of duodenum, due to multiple causes, including bacteria (Marshall and Warren 1984; Lykoudes 1958), chewing gum, tobacco smoking, not eating properly, blood group, spice (NADDIC- National Alcohol and Drug Dependence Industry Committee), chronic stress (Kim et al. 2007) and gender differences (Andes et al. 2008). Specific protection of estrogen against gastric –acid induced duodenal injury was reported (Andes et al. 2008). "
"After Helicobacter pylori was identified in human gastric mucosa by Warren and Marshall, this bacterium was found to be associated with gastritis, peptic ulcers, gastric adenocarcinoma and mucosa-associated lymphoid tissue lymphoma (Ruiz-Bustos et al. 2001; Vinette et al. 2004). In particular, H. pylori infection (HI) is a major causal factor in peptic ulcer, and recurrence is virtually prevented by eradicating this bacterium (Kim et al. 2002). Although there is a high probability of HI in peptic ulcer cases, such infection is not sufficient alone for peptic ulcer to develop: many infected people do not develop ulcers, and some gastric ulcer patients are H. pylori-negative (Aoyama et al. 2000; Velin and Michetti 2006). "
[Show abstract][Hide abstract] 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.
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