Regulatory T cells curb unwanted immune responses and regulate responses to microflora and it is now clear that regulatory T cells play an important role in a number of chronic inflammatory diseases of the gut. First, regulatory T cells are crucial in controlling immune responses to gastric autoantigens and thus preventing autoimmune gastritis and pernicious anemia. Second, regulatory T cells may modulate the response to Helicobacter pylori, thus affecting the ability of the immune system to clear the pathogen and mediate damage to the gastric mucosa. Finally, regulatory T cells play an important role in preventing damaging inflammatory responses to commensal organisms in the lower gut, thus guarding against inflammatory bowel diseases. In the present review, we examine the actions of regulatory T cells in the gut and conclude that further understanding of regulatory T cell biology may lead to new therapeutic approaches to chronic gastrointestinal disease.
In several autoimmune diseases, including multiple sclerosis (MS), a compromised regulatory T cell (Treg) function is believed to be critically involved in the disease process. In vitro, the biologically active metabolite of vitamin D has been shown to promote Treg development. A poor vitamin D status has been linked with MS incidence and MS disease activity
Plasma and gastric tissue selenium levels in patients with Helicobacter pylori infection
Résumé / Abstract
Goals: We investigated plasma and gastric mucosal selenium levels in patients with Helicobacter pylori (HP)-associated histopathologic findings in their gastric antral mucosa. Study: Before and after a successful HP eradication therapy, we quantitated the plasma and antral selenium levels in patients with HP-associated chronic antral gastritis using atomic absorption flame emission spectrometry. The same measurements were done in patients with dyspeptic complaints who had normal antral histology and negative urease test. Results: Thirty-four patients were studied, of whom 24 had HP-associated chronic antral gastritis confirmed by histology and positive urease test; the control group included 10 healthy patients. There was no difference between the groups with regard to age, gender, and number of smokers. All patients with HP infection were diagnosed with diffuse antral gastritis. Histopathology showed that 11 (49%) had some degree of atrophy. Of the 11 patients, 7 were classified as having chronic atrophic gastritis (CAG) without intestinal metaplasia (IM), 4 had IM, and none had dysplasia. The plasma concentrations of selenium were found to be very similar in controls and HP-infected subjects (68.0 ± 25.97 μg/L and 71 ± 32.9 μg/L, respectively; p > 0.05). The antral biopsy samples of the patients with HP-associated gastritis contained significantly higher levels of tissue selenium than the controls (20.17 ± 19.74 μg/g and 2.83 ± 1.42 μg/g, respectively; p < 0.05). Also, it was shown that antral tissue selenium levels decrease after successful HP eradication therapy (20.17 ± 19.4 μg/g and 7.4 ± 4.56 μg/g, respectively; t < 0.05). The patients with HP gastritis were assigned to mild, moderate, and severe gastritis groups, according to the histopathologic degree of inflammation present. The antral gastric selenium levels were significantly higher in patients with moderate and severe HP gastritis (21.13 ± 22.5 μg/g and 22.81 ± 17.35 μg/g, respectively) than in patients with mild gastric inflammation (9.53 ± 10.3 μg/g; p < 0.05). The selenium concentrations in the biopsies of patients with CAG were significantly lower than in those with HP gastritis who did not have CAG (9.45 ± 6.44 μg/g vs. 19.13 ± 22.48 μg/g, respectively; p < 0.05). Conclusions: Selenium accumulates in gastric tissue when it is needed, as is the case in HP-related antral inflammation. This reactive increase in gastric mucosal selenium seems to disappear in the presence of precancerous gastric lesions in the setting of HP-associated gastritis.
The effects of selenium deficiency on the responses to Candida albicans infection were examined in mice. When selenium-deficient and selenium-supplemented mice were given i.v. injections of 0.1 ml suspensions of 1 x 105 or 5 x 104 C. albicans in 0.9% sterile saline, deaths in the selenium-deficient animals started after 2.5–3.5 d compared with 7–8.5 d in the selenium-supplemented animals. Further studies demonstrated that 3 d after an i.v. injection of 1 x 105 C. albicans, significantly more of the microorganisms were found in the kidneys (P < 0.001), livers (P < 0.025) and spleens (P < 0.01) of the selenium-deficient mice compared with the same organs of selenium-supplemented animals. Selenium deficiency was also demonstrated to impair the ability of mouse neutrophils to kill C. albicans in in vitro tests. The possible relationships of this defect in function to decreased resistance to C. albicans infection is discussed.
Summary We measured the serum selenium concentration in 64 patients with uncomplicated viral (n=33) or bacterial (n=31) infections during the acute stage of infection, during the early convalescent phase and after a minimum recovery period of three weeks and compared it to serum iron values. Both selenium (mean ± SEM: 70.3±2.3 µg/l vs 79.4±2.2 µg/l, p<0.0001) and iron (8.4±0.8 µg/l vs 16.7±0.9 µg/l, p<0.0001) concentrations showed significant depressions in the acute stage of infection compared with the values after the recovery. The reduction of serum selenium did not correlate with the severity of infection measured by fever. We conclude that acute infections decrease serum selenium levels regardless of the infective agent. The changes are of interest because of the possible connection between selenium and the immune system.
The content of polyunsaturated fatty acids, especially eicosapentaenoic acid, in serum cholesterol esters and phospholipids was positively correlated with selenium concentration.
Haematologica. 2005 May;90(5):585-95.
Role of autoimmune gastritis, Helicobacter pylori and celiac disease in refractory or unexplained iron deficiency anemia.
BACKGROUND AND OBJECTIVES: Conventional endoscopic and radiographic methods fail to identify a probable source of gastrointestinal blood loss in about one third of males and post-menopausal females and in most women of reproductive age with iron deficiency anemia (IDA). Such patients, as well as subjects refractory to oral iron treatment, are often referred for hematologic evaluation. DESIGN AND METHODS: Patient clinic, screened for non-bleeding gastrointestinal conditions including celiac disease (antiendomysial antibodies), autoimmune atrophic gastritis (hypergastrinemia with strongly positive antiparietal cell antibodies) and H. pylori infection (IgG antibodies confirmed by urease breath test). RESULTS: The mean age of all subjects was 39+/-18 years, and 119 of 150 were females. We identified 8 new cases of adult celiac disease (5%). Forty IDA patients (27%) had autoimmune atrophic gastritis of whom 22 had low serum vitamin B12 levels. H. pylori infection was the only finding in 29 patients (19%), but was a common co-existing finding in 77 (51%) of the entire group. Refractoriness to oral iron treatment was found in 100% of patients with celiac disease, 71% with autoimmune atrophic gastritis, 68% with H. pylori infection, but only 11% of subjects with no detected underlying abnormality. H. pylori eradication in previously refractory IDA patients in combination with continued oral iron therapy resulted in a significant increase in hemoglobin from 9.4+/-1.5 (mean +/- 1SD) before, to 13.5+/-1.2 g/ dL (p<0.001 by paired t test) within 3 to 6 months. INTERPRETATION AND CONCLUSIONS: The recognition that autoimmune atrophic gastritis and H. pylori infection may have a significant role in the development of unexplained or refractory IDA in a high proportion of patients should have a strong impact on our daily practice of diagnosing and managing IDA.
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