Identification of a Correlation between Helicobacter pylori Infection and Graves’ Disease

U.O.C. di Medicina Interna, San Giovanni Bosco Hospital, ASL Na 1 Centro, Naples, Italy.
Helicobacter (Impact Factor: 4.11). 12/2010; 15(6):558-62. DOI: 10.1111/j.1523-5378.2010.00802.x
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Viral and bacterial antigens have been suspected to be able to mimic the antigenic profile of the thyroid cell membrane and to play an important role in the onset of the autoimmune diseases, such as Graves' disease and Hashimoto thyroiditis. The Helicobacter pylori infection is worldwide diffused and is present in the developed countries up to 50% of the population. The presence of the cytotoxin-associated gene A antigens identifies the most virulent strains of the bacterium. Previous studies have demonstrated the possible correlation between the Helicobacter pylori and Hashimoto's thyroiditis but these results are controversial.
We studied the prevalence rate of this bacterium in the Graves' disease and two selected subgroups such as the hyperthyroid patients, at the first time of diagnosis, and the euthyroid methimazole-treated patients.
We analyzed Helicobacter pylori in fresh stool samples with an enzyme immunoassay method and the presence of cytotoxin-associated gene A antigens with a serological test.
Our results show that a significative increased rate of prevalence is present in Graves' patients, when the disease is ongoing, with an overall prevalence of the strains expressing the cytotoxin-associated gene A antigens compared to the control group.
The association between the Helicobacter pylori and Graves' disease suggests a possible role of this bacterium in the onset and/or the maintenance of the disease.

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    • "The results suggest that an autoimmune reaction might be involved in the pathogenesis of not only H. pylori-associated gastrointestinal disorders, but also extra-intestinal autoimmune disorders. Autoantigens reported to be involved in diverse autoimmune disorders associated with H. pylori infection include carbonic anhydrase II similar alpha carbonic anhydrase of H. pylori in autoimmune pancreatitis,20 anti-CagA antibody, anti-HSP 65 antibody, and anti-HSP 60 antibody in artherosclerosis,21-23 anti-CagA antibody in Graves disease,24 anti-platelet glycoprotein antibody in immune thrombocytopenic purpura,25 proteins from endothelial or smooth muscle cells against CagA in hypertension,26 and HSP 60 of H. pylori associated with Sjogren syndrome.27 A healthy human body has immune regulatory systems including Treg cells. "
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    ABSTRACT: Purpose This study tried to identify novel gastric autoimmune antigens that might be involved in aggravating the atrophic gastritis among patients with Helicobacter pylori infection using two-dimensional immunoblotting analysis. Materials and Methods Proteins from gastric mucosal antrectomy specimens and AGS cells (gastric adenocarcinoma cell lines derived from a Caucasian patient who had received no prior therapy) were 2-dimensionally immunoblotted separately with a pool of 300 sera from H. pylroi-infected patients at Gyeongsang National University Hospital. Results Thirty-eight autoantigenic proteins including alcohol dehydrogenase [NADP+], alpha enolase, gastrokine-1, gastric triacylglycerol lipase, heat shock 70 kDa protein 1, and peroxiredoxin-2 were identified in the gastric mucosal tissue. Fourteen autoantigenic proteins including programmed cell death 6-interacting protein, serum albumin and T-complex protein 1 subunit gamma were identified in the AGS cells. Albumin, alpha-enolase, annexin A3, cytoplasmic actin 1, heat shock cognate 71 kDa protein and leukocyte elastase inhibitor were commonly observed autoantigenic proteins in both gastric mucosal tissue and AGS cells. Alpha-enolase, glutathione S-transferase P, heat shock cognate 71 kDa protein, heat shock 70 kDa protein 1, human mitochondrial adenosine triphosphate synthase (ATP) subunit beta, mitochondrial 60 kDa heat shock protein, peroxiredoxin-2, 78 kDa glucose-regulated protein precursor, tyrosine-protein phosphatase non-receptor type 11 and Tryptophan-Aspartic acid (WD) repeat-containing protein 1 showed 60% or higher amino acid positivity. Conclusion These newly identified gastric autoimmune antigens might be useful in the control and prevention of gastroduodenal disorders, and might be valuable in breaking the vicious circle that exists in gastroduodenal disorders if their pathophysiological roles could be understood in the progress of chronic atrophic gastritis, gastroduodenal ulcers, intestinal metaplasia, and gastric carcinogenesis.
    Yonsei medical journal 11/2013; 54(6):1342-52. DOI:10.3349/ymj.2013.54.6.1342 · 1.29 Impact Factor
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    • "In addition to gastrointestinal disease, H. pylori is associated with several autoimmune diseases, including idiopathic thrombocytopenic purpura (ITP), Sjögren syndrome, systemic sclerosis [19], Graves' disease [20], and autoimmune pancreatitis [21]. Given this association with autoimmune diseases, we hypothesized that H. pylori might induce systemic immunological changes. "
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    ABSTRACT: Background. Helicobacter pylori chronically colonizes gastric/duodenal mucosa and induces gastroduodenal disease and vigorous humoral and cellular immune responses. Methods. In order to clarify the immunological changes induced by this infection, we determined the percentage and, as indicated, ratios of the following cells in peripheral blood of 45 H. pylori-infected patients and 21 control subjects: CD4+ T cell, CD8+ T cells, T helper 1 cells (Th1), T helper 2 cells (Th2), CD4+CD25+ T cells, Foxp3+ regulatory T cells (Tregs), CD4/CD8 ratio, and Th1/Th2 ratio. Results. The percentage of CD8+ T cells was significantly lower in H. pylori-infected patients (mean ± SD; 18.0 ± 7.1%) compared to control subjects (mean ± SD; 23.2 ± 7.8%) (P < 0.05). The CD4/CD8 ratio was significantly higher in H. pylori-infected patients (mean ± SD; 3.1 ± 2.4) compared to control subjects (mean ± SD; 2.1 ± 1.0) (P < 0.05). The Th1/Th2 ratio was significantly lower in H. pylori-infected patients (mean ± SD; 10.0 ± 8.5) compared to control subjects (mean ± SD; 14.5 ± 9.0) (P < 0.05). The percentage of CD4+CD25+ T cells in H. pylori-infected patients (mean ± SD; 13.2 ± 6.2%) was significantly higher than that in control subjects (mean ± SD; 9.8 ± 3.4%) (P < 0.05). However, there was no significant difference in Tregs. Conclusion. Tregs did not decrease, but the activation of humoral immunity and Th2 polarization were observed in the peripheral blood of H. pylori-infected patients. In some cases, these changes may induce systemic autoimmune diseases.
    Gastroenterology Research and Practice 03/2012; 2012(8390):819842. DOI:10.1155/2012/819842 · 1.75 Impact Factor
  • Helicobacter 08/2011; 16(4):338. DOI:10.1111/j.1523-5378.2011.00843.x · 4.11 Impact Factor
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