Role of Helicobacter pylori infection in autoimmune systemic rheumatic diseases

Abstract

The relationship between infection and autoimmunity has been increasingly defined over the last 20 years. The systemic rheumatic diseases are characterized by dysregulation of the immune system resulting in a loss of tolerance to self-antigen. The exact etiology for the majority of these diseases is unknown; however, a complex combination of host and environmental factors are believed to play a pivotal role. Helicobacter pylori (H. pylori) is one of the most widely studied infectious agents proposed as agents triggering autoimmune response. The persistent presence of H. pylori in the gastric mucosa results in chronic immune system activation with ongoing cytokine signaling, infiltration of gastric mucosa by neutrophils, macrophages, lymphocytes, as well as production of antibodies and effector T-cells. Various mechanisms have been proposed in an attempt to explain the extra-intestinal manifestations of H. pylori infections. These include: molecular mimicry, endothelial cell damage, superantigens and microchimerism. I performed a systematic literature review using the keywords “rheumatoid arthritis”, “Sjögren’s syndrome”, “systemic sclerosis”, “systemic lupus erythematosus”, “Helicobacter pylori” and “pathogenesis”. A systematic literature search was carried out in MEDLINE; EMBASE; Cochrane Library and ACR/EULAR meeting abstracts. In systemic rheumatic diseases H. pylori infection prevalence alone should not be expected to provide sufficient evidence for or against a pathologic role in the disease. In this article I review studies examining the potential involvement of H. pylori infection in autoimmune systemic rheumatic diseases. Further studies of the immunological response to H. pylori and its role in the pathogenesis of systemic rheumatic diseases are warranted.

Keywords: Rheumatoid arthritis; Sjögren’s syndrome; Systemic sclerosis; Systemic lupus erythematosus; Helicobacter pylori; Pathogenesis

Core tip: The exact etiology of systemic rheumatic diseases is unclear, but it has long been suggested that exposure to certain environmental agents, such as bacterial infection, in genetically predisposed individuals may be the trigger for the initiation of autoimmune processes. Because of its prevalence and ability to affect human immune function, many researchers have hypothesized that Helicobacter pylori (H. pylori) might contribute to the systemic rheumatic diseases development. I summarize the current state of knowledge about H. pylori role in autoimmune systemic rheumatic diseases and the possible mechanisms by which H. pylori exposures might induce pathological processes.