Role of Helicobacter pylori Infection in Autoimmune Diseases

Sarfaraz Ahmed Hasni


Curr Opin Rheumatol. 2012;24(4):429-434. 

In This Article

Abstract and Introduction


Purpose of review The etiology of most autoimmune diseases remains elusive. Prevailing evidence suggests an environmental trigger in a genetically susceptible individual. Helicobacter pylori (H. pylori) have managed to survive in a hostile environment in their host for long period and have evaded eradication by the immune system. Its chronic interaction with the immune system and the ubiquitous presence worldwide makes H. pylori an ideal candidate to study as a trigger of autoimmune phenomena. In this review, we would present data regarding the interplay between H. pylori and various components of the immune system and its association with various autoimmune diseases.
Recent findings Strong associations of H. pylori with some autoimmune diseases such as immune thrombocytopenia have been found; but most other autoimmune disease studies have revealed conflicting data. The chronic survival of H. pylori in humans is possible because of an overall downregulation of the body's immune response. In addition to this overall effect on the immune system, there are clinical and epidemiological data suggestive of H. pylori infection having a protective role in some autoimmune diseases.
Summary Based on our review H. pylori status should be checked and treated only in certain autoimmune diseases such as ITP. For the majority of the autoimmune diseases, the role of H. pylori remains controversial signifying need for further research.


Autoimmune diseases vary significantly in their clinical presentations, but share the same pathophysiological mechanism resulting from a loss of self-tolerance. Despite significant advances in our understanding and management of autoimmune diseases, factors leading to this loss of self-tolerance are still poorly understood.

Studies in twins with autoimmune diseases show a much higher concordance rate in identical twins compared with nonidentical twins, indicative of a clear genetic component. However, the concordance rate is not 100% and the majority of identical twins with autoimmune diseases have a nonaffected twin.[1] In a recent review[2] monozygotic twin concordance rate was reported to be as low as 4.2 for systemic sclerosis. This suggests a second environmental factor triggering immune dysregulation in these genetically susceptible hosts leading to autoimmune diseases. Among the various possible environmental triggers, studies looking at the role of various infectious agents have been most promising.[3•] Microbial organisms are considered to be likely triggers of autoimmunity because of their ubiquitous presence in the environment and their interaction with the immune system. There are several proposed mechanisms by which microbial organisms can lead to loss of self-tolerance; such as molecular-mimicry, when shared amino acid sequences between microbial antigens and host proteins leads to a more generalized triggering of immune response against both the host proteins and microbial antigens.[4] Other proposed mechanisms leading to triggering of autoimmunity include polyclonal activation, epitope spread, bystander activation and superantigens.[5] Of the various bacteria and viruses proposed as agents triggering autoimmunity, Helicobacter pylori (H. pylori) is one of the most widely studied. This is because of attributes unique to H. pylori such as prolonged survival in host environment, worldwide prevalence, and its complex interactions with the host immune system. In this review, we will look at the interactions between H. pylori and the immune system in general and the role of H. pylori in individual autoimmune diseases.


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