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Review
. 2011 Oct;17(7):621-7.
doi: 10.1111/j.1601-0825.2011.01796.x. Epub 2011 Mar 29.

Helicobacter pylori and autoimmune diseases

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Review

Helicobacter pylori and autoimmune diseases

S Hasni et al. Oral Dis. 2011 Oct.

Abstract

Helicobacter pylori (H. pylori) is a widely prevalent microbe, with between 50 and 80% of the population infected worldwide. Clinically, infection with H. pylori is commonly associated with peptic ulcer disease, but many of those infected remain asymptomatic. H. pylori has evolved a number of means to affect the host immune response and has been implicated in many diseases mitigated by immune dysregulation, such as immune thrombocytopenic purpura (ITP), atrophic gastritis, and mucosa associated lymphoid tissue (MALT) lymphoma. Autoimmune diseases, such as systemic lupus erythematosus, rheumatoid arthritis, and Sjogren's syndrome, are the result of a dysregulated host immune system which targets otherwise healthy tissues. The exact etiology of autoimmune diseases is unclear, but it has long been suggested that exposure to certain environmental agents, such as viral and bacterial infection or chemical exposures, in genetically susceptible individuals may be the catalyst for the initiation of autoimmune processes. Because of its prevalence and ability to affect human immune function, many researchers have hypothesized that H. pylori might contribute to the development of autoimmune diseases. In this article, we review the available literature regarding the role of chronic H. pylori infection in various autoimmune disease states.

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References

    1. Amedei A, Bergman MP, Appelmelk BJ, et al. Molecular mimicry between Helicobacter pylori antigens and H+, K+ – adenosine triphosphatase in human gastric autoimmunity. J Exp Med. 2003;198:1147–1156. - PMC - PubMed
    1. Aragona P, Magazzu G, Macchia G, et al. Presence of antibodies against Helicobacter pylori and its heat-shock protein 60 in the serum of patients with Sjogren’s syndrome. J Rheumatol. 1999;26:1306–1311. - PubMed
    1. Asahi M, Azuma T, Ito S, et al. Helicobacter pylori CagA protein can be tyrosine phosphorylated in gastric epithelial cells. J Exp Med. 2000;191:593–602. - PMC - PubMed
    1. Azevedo NF, Huntington J, Goodman KJ. The epidemiology of Helicobacter pylori and public health implications. Helicobacter. 2009;14(Suppl 1):1–7. - PubMed
    1. Bach JF. Infections and autoimmune diseases. J Autoimmun. 2005;25(Suppl):74–80. - PubMed

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