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World J Gastroenterol. Jan 21, 2014; 20(3): 613-629
Published online Jan 21, 2014. doi: 10.3748/wjg.v20.i3.613
Helicobacter pylori and autoimmune disease: Cause or bystander
Daniel S Smyk, Andreas L Koutsoumpas, Maria G Mytilinaiou, Dimitrios P Bogdanos, Institute of Liver Studies, Division of Transplantation Immunology and Mucosal Biology, King’s College Hospital, School of Medicine, King’s College London, London SE5 9RS, United Kingdom
Andreas L Koutsoumpas, Eirini I Rigopoulou, Dimitrios P Bogdanos, Department of Medicine, Faculty of Medicine, School of Health Sciences, University of Thessaly, Biopolis, 41110 Larissa, Greece
Lazaros I Sakkas, Department of Rheumatology, Faculty of Medicine, School of Health Sciences, University of Thessaly, Biopolis, 41110 Larissa, Greece
Dimitrios P Bogdanos, Cellular Immunotherapy and Molecular Immunodiagnostics, Biomedical Section, CEntre for REsearch and TEchnology Hellas (CE.R.T.H.)/Institute for REsearch and Technology-THessaly (I.RE.TE.TH), 60361 Thessaloniki, Greece
Author contributions: Smyk DS and Bogdanos DP conducted the literature review, wrote the first and subsequent drafts, and edited the manuscript; Koutsoumpas AL, Mytilinaiou MG, Rigopoulou EI and Sakkas LI significantly contributed to the writing and editing of the manuscript.
Correspondence to: Dimitrios P Bogdanos, MD, PhD, Department of Medicine, Faculty of Medicine, School of Health Sciences, University of Thessaly, Mezourlo Campus, Biopolis, 41110 Larissa, Greece.
Telephone: +30-241-3502766 Fax: +30-241-3502813
Received: September 30, 2013
Revised: November 25, 2013
Accepted: December 5, 2013
Published online: January 21, 2014


Helicobacter pylori (H. pylori) is the main cause of chronic gastritis and a major risk factor for gastric cancer. This pathogen has also been considered a potential trigger of gastric autoimmunity, and in particular of autoimmune gastritis. However, a considerable number of reports have attempted to link H. pylori infection with the development of extra-gastrointestinal autoimmune disorders, affecting organs not immediately relevant to the stomach. This review discusses the current evidence in support or against the role of H. pylori as a potential trigger of autoimmune rheumatic and skin diseases, as well as organ specific autoimmune diseases. We discuss epidemiological, serological, immunological and experimental evidence associating this pathogen with autoimmune diseases. Although over one hundred autoimmune diseases have been investigated in relation to H. pylori, we discuss a select number of papers with a larger literature base, and include Sjögrens syndrome, rheumatoid arthritis, systemic lupus erythematosus, vasculitides, autoimmune skin conditions, idiopathic thrombocytopenic purpura, autoimmune thyroid disease, multiple sclerosis, neuromyelitis optica and autoimmune liver diseases. Specific mention is given to those studies reporting an association of anti-H. pylori antibodies with the presence of autoimmune disease-specific clinical parameters, as well as those failing to find such associations. We also provide helpful hints for future research.

Key Words: Autoimmunity, Helicobacter pylori, Infection, Gastritis, Mimicry, Rheumatology

Core tip: Multiple infectious agents have been implicated in the development of autoimmune disease. Helicobacter pylori is one pathogen which has been linked with multiple autoimmune diseases. This review will critically discuss a select few studies which have a larger evidence base, both in terms of positive and negative findings.


Autoimmune diseases arise from the interaction of genetic susceptibility and environmental exposures[1-4]. Among environmental exposures, infectious triggers have been implicated and studied extensively[1,5]. Infectious agents include bacteria, viruses and parasites, and may also consist of those organisms which comprise the normal flora[5]. Several mechanisms by which infectious agents may cause autoimmune disease have been proposed[6,7]. These include molecular mimicry[8-10], epitope spreading, bystander effect[11,12], microbial super-antigens, immune complex formation[13], MHC class II expression on non-immune cells[14], direct inflammatory damage[13], high levels of pro-inflammatory cytokines such as interferon (IFN)-γ[10], and T-regulatory/Th17 imbalance.

Among infectious agents implicated, Helicobacter pylori (H. pylori) has received particular attention, in that it has been implicated in both organ specific and non-organ specific autoimmune disease[15]. As gastric disease in relation to H. pylori has been discussed extensively in multiple reviews and studies[16-18], it will not be discussed in this review. Likewise, multiple other autoimmune conditions have been linked with H. pylori, with evidence bases of varying content. In fact, amongst the autoimmune or autoimmune related diseases listed by AARDA (American Autoimmune Related Diseases Association,, 95 have been studied sporadically or systematically in regard to their connection with H. pylori, while among the remaining 61 there are no studies (yet) in Pubmed (search up to 29 September 2013) (Tables 1 and 2). Therefore, this review will discuss selected autoimmune conditions, both organ specific and non-organ specific, which have an evidence base (positive or negative) in relation to H. pylori infection. Amongst the non-organ specific autoimmune disorders, we thoroughly discuss immune thrombocytopenic purpura (ITP) and autoimmune rheumatic diseases, such as rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), Sjögren syndrome (SjS), systemic sclerosis (SSc). Amongst the organ specific diseases linked with H. pylori, autoimmune thyroid disease (AiTD), and multiple sclerosis (MS)/neuromyelitis optica (NMO) are discussed, as well as autoimmune liver diseases such as primary biliary cirrhosis (PBC), primary sclerosing cholangitis (PSC) and autoimmune hepatitis (AIH). Although a wealth of literature is available for some conditions, we present selected papers that highlight the current findings, or lack thereof. It will become apparent that the evidence in support of H. pylori as a cause of some autoimmune conditions varies from one condition to the next.

Table 1 Autoimmune diseases or autoimmune disease-related disorders which have been studied for their possible (direct or indirect) relation with Helicobacter pylori infection.
AID or AID-related disorders linked to H. pyloriAID or AID-related disorders linked to H. pylori
1Alopecia areata49Juvenile diabetes (Type 1 diabetes)
2Antiphospholipid syndrome50Kawasaki syndrome
3Autoimmune angioedema51Leukocytoclastic vasculitis
4Autoimmune hepatitis52Lichen planus
5Autoimmune hyperlipidemia53Linear IgA disease
6Autoimmune hemolytic anemia54Lupus (SLE)
7Autoimmune myocarditis55Microscopic polyangiitis
8Autoimmune oophoritis56Mixed connective tissue disease
9Autoimmune pancreatitis57Mooren’s ulcer
10Autoimmune polyglandular syndromes58Multiple sclerosis
11Autoimmune thrombocytopenic purpura59Myositis
12Autoimmune thyroid disease60Narcolepsy
13Autoimmune urticaria61Neuromyelitis optica (Devic’s)
14Axonal and neuronal neuropathies62Neutropenia
15Behcet’s disease63Ocular cicatricial pemphigoid
16Bullous pemphigoid64Optic neuritis
17Cardiomyopathy65Palindromic rheumatism
18Celiac disease66Pars planitis (peripheral uveitis)
19Chagas disease67Pemphigus
20Chronic inflammatory demyelinating polyneuropathy68Peripheral neuropathy
21Chronic recurrent multifocal osteomyelitis69Perivenous encephalomyelitis
22Crohn’s disease70Pernicious anemia
23Cogans syndrome71Polyarteritis nodosa
24Demyelinating neuropathies72Polymyalgia rheumatica
25Dermatitis herpetiformis73Polymyositis
26Dermatomyositis74Primary biliary cirrhosis
27Devic’s disease (neuromyelitis optica)75Primary sclerosing cholangitis
28Eosinophilic esophagitis76Psoriasis
29Eosinophilic fasciitis77(Idiopathic) pulmonary fibrosis
30Erythema nodosum78Pyoderma gangrenosum
31Experimental allergic encephalomyelitis79Raynaud’s phenomenon
32Fibromyalgia80Reactive Arthritis
33Fibrosing alveolitis81Reiter’s syndrome
34Giant cell arteritis (temporal arteritis)82Relapsing polychondritis
35Giant cell myocarditis83Rheumatoid arthritis
37Goodpasture’s syndrome85Scleroderma (systemic sclerosis)
38Graves’ disease86Sjogren’s syndrome
39Guillain-Barre syndrome87Temporal arteritis/Giant cell arteritis
40Hashimoto’s thyroiditis88Thrombocytopenic purpura
41Henoch-Schonlein purpura89Transverse myelitis
42Hypogammaglobulinemia idiopathic thrombocytopenic purpura90Type 1 diabetes
43IgA nephropathy91Ulcerative colitis
44IgG4-related sclerosing disease92Undifferentiated connective tissue disease
45Immunoregulatory lipoproteins93Uveitis
46Inclusion body myositis94Vasculitis (other forms)
47Interstitial cystitis95Vesiculobullous dermatosis
48Juvenile arthritis
Table 2 Autoimmune diseases or autoimmune diseases-related disorders which have not been studied for their possible (direct or indirect) relation with Helicobacter pylori infection.
AID or AID-related disorders not linked to H. pylori
1Acute Disseminated Encephalomyelitis
2Acute necrotizing hemorrhagic leukoencephalitis
3Addison's disease
6Ankylosing spondylitis
7Anti-GBM/Anti-TBM nephritis
8Autoimmune aplastic anemia
9Autoimmune dysautonomia
10Autoimmune immunodeficiency
11Autoimmune inner ear disease
12Autoimmune retinopathy
13Balo disease
14Castleman disease
15Chronic fatigue syndrome
16Churg-Strauss syndrome
17Cicatricial pemphigoid/benign mucosal pemphigoid
18Congenital heart block
19Coxsackie myocarditis
20CREST disease
21Essential mixed cryoglobulinemia
22Discoid lupus
23Dressler’s syndrome
25Evans syndrome
26Granulomatosis with Polyangiitis (formerly called Wegener’s Granulomatosis)
27Hashimoto’s encephalitis
28Herpes gestationis
29Juvenile myositis
30Lambert-Eaton syndrome
31Lichen sclerosus
32Ligneous conjunctivitis
33Lyme disease,
34(Chronic) Meniere’s disease
35Mucha-Habermann disease
36Myasthenia gravis
37Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcus
38Paraneoplastic cerebellar degeneration
39Paroxysmal nocturnal hemoglobinuria
40Parry Romberg syndrome
41Parsonage-Turner syndrome
42POEMS syndrome
43Postmyocardial infarction syndrome
44Postpericardiotomy syndrome
45Progesterone dermatitis
46Psoriatic arthritis
47Pure red cell aplasia
48Reflex sympathetic dystrophy
49Restless legs syndrome
50Retroperitoneal fibrosis
51Rheumatic fever
52Schmidt syndrome
54Sperm and testicular autoimmunity
55Stiff person syndrome
56Subacute bacterial endocarditis
57Susac’s syndrome
58Sympathetic ophthalmia
59Takayasu’s arteritis
60Tolosa-Hunt syndrome

Several mechanisms of pathogen-induced autoimmunity have been described in studies of H. pylori-induced autoimmunity[19]. We briefly discuss some of these papers, starting with the study by Jackson and colleagues[20]. These investigators found that chronic H. pylori infection was associated with an increased risk of an elevated serum C-reactive protein, indicating an ongoing inflammatory state. This chronic inflammation may result in ongoing antigenic stimulation, and induces a systemic inflammatory response, and therefore extra-gastrointestinal disease[20]. However, such hypotheses are not accompanied by solid experimental data. We need to emphasize that this, as well as most other studies investigating the role of H. pylori, speculates rather than demonstrates a pathogenic role for this bacterium. Another study found that molecular mimicry of H. pylori antigens activated cross-reactive T cells in autoimmune gastritis[21]. H. pylori components (especially urease) have been shown to activate B cells to produce IgM rheumatoid factor, anti-dsDNA, and anti-phospholipid choline antibodies[22]. The former studies belong to those few (compared to the great majority of the studies) that to some extent provide a mechanistic approach as to how the pathogen can inflict loss of immunological tolerance, which is an important component for the initiation of antigen-driven autoimmunity. Similar mechanisms have been proposed in relation to heat shock protein (hsp) 60[23]. Another piece of evidence which can support the major role of H. pylori in the development of autoimmune diseases (and not just in the induction of autoantibodies) stems from studies on animal models of autoimmune diseases. Infection of male C57BL/6 mice with H. pylori can induce a disease that resembles human PBC[24]. However, most animal models of autoimmune diseases do not rely on H. pylori infection for the induction of the disease or do not provide data to support that this pathogen is needed for disease development. Most of the mechanisms discussed in the literature remain as hypotheses that require more extensive investigation.


The pathogenetic evidence linking H. pylori with autoimmune rheumatic diseases varies amongst diseases. For example, while there are a reasonable number of studies investigating this topic in SjS, the data stemming from SLE are relatively few and inconsistent. There are several explanations that could account for the great variation in the number of the studies conducted amongst diseases. Some studies are rare and translational research is difficult to perform, as in for example the case of SSc. Other diseases do not have reliable animal models, and in these disorders it has been almost impossible to assess the role of infectious agents in the induction of autoimmunity. Also, for some diseases the prevailing idea amongst researchers has been that H. pylori is not an attractive etiologic agent, and this has prevented more research in this topic over the years. Nevertheless, epidemiological, serological and clinical studies have been performed to some extent and are reviewed herein.

Sjögren’s syndrome

SjS is an autoimmune condition characterized by lymphoid cell infiltration and destruction of exocrine glands[19]. As lacrimal and salivary glands are most affected, a link with H. pylori has been made given its prevalence in the oral cavity[19], which may be associated with anti-H. pylori antibodies[25].

Aragon et al[23] found that 79.4% of SjS patients had anti-H. pylori antibodies, and that 88.2% had anti-hsp60. This was significantly higher than other autoimmune controls (18.2% with anti-H. pylori; 27.3% with anti-hsp60), and healthy controls (48.8% anti-H. pylori; 37.2% anti-hsp60)[23]. El Miedany et al[26] failed to find statistically significant differences in the prevalence of anti-H. pylori antibodies between patients with primary and secondary SjS (80.6% vs 71% for IgG, and 47.2% vs 38.7% for IgA, respectively). However, anti-H. pylori antibodies were significantly less prevalent in patients with connective tissue disorders lacking sicca syndrome symptomatology (60.9% for IgG and 19.6% for IgM). The lowest prevalence of IgG and IgM anti-H. pylori antibodies was found in normal controls (56.3% for IgG and 12.5% for IgM, respectively)[26]. Similar results have been found in further studies[27], but contradictory data have been provided in others[28]. A study by the group of Theander[28] examined the prevalence of H. pylori in a Swedish cohort of 164 SjS patients, and found that 45% were seropositive for H. pylori infection, including 23% with anti-CagA antibodies. However, these rates were lower than those seen in a control group of orthopedic outpatients without autoimmune conditions, and similar to rates found among healthy individuals[28]. That group therefore concluded that H. pylori infection was not linked with SjS[28].

Some studies have attempted to link evidence of H. pylori infection with clinical features of SjS. For example, El Miedany et al[26] have found that there is a significant correlation between (IgG and IgM) anti-H. pylori antibody seropositivity and the presence of primary and secondary SjS, as well as various clinical parameters. Logistic regression analysis has revealed that the presence of IgG anti-H. pylori antibodies significantly correlates with age, disease duration and global score for disease status.

Another possible link between SjS and H. pylori may be found in mucosa-associated lymphoid tissue (MALT) lymphomas that may arise from chronic antigenic stimulation (i.e., chronic infection and/or autoimmune disease). H. pylori was detected in gastric tissue from MALT, and interestingly, there is an increased incidence of MALT lymphomas and marginal zone B cell neoplasms in SjS[29]. It is possible that H. pylori eradication in SjS may result in decreased incidence of MALT, as is the case for gastric MALT lymphomas[30-32]. Further studies regarding the prevalence of H. pylori in SjS in different populations are currently needed, in addition to monitoring for H. pylori in at-risk individuals.

Rheumatoid arthritis

Sir James Paget was one of the very first to consider the possibility that what is now known as rheumatoid arthritis may indeed be caused by microbial infections. In 1853, Paget hypothesized that all diseases that manifest their symptoms symmetrically, such as “the deformities of chronic rheumatism”, must be blood-borne and could be caused by a demonstrable virus. H. pylori has been considered one of the infectious agents linked to RA; however, the data do not support this. An increased incidence of peptic ulcer disease in RA patients is most likely related to the use of non-steroidal anti-inflammatory drugs[33]. Yamanishi et al[22] found increased IgM rheumatoid factor in B cells chronically stimulated with H. pylori urease. However, several studies demonstrated that there is a lower prevalence of H. pylori in RA patients, and other studies found the prevalence of H. pylori to be similar to that of the healthy controls[27,34,35]. After H. pylori eradication, no change in RA symptoms was reported by several studies[36-38], although improvement was noted in others[39,40]. Currently, the data are mixed regarding RA and H. pylori, and it appears that the link is weak.

Systemic lupus erythematosus

H. pylori prevalence has been studied in patients with SLE, but the results vary amongst reports. A recent study has failed to find significantly higher prevalence of anti-H. pylori antibodies in SLE patients compared to controls[41]. Of note, this study showed an increased prevalence of anti-H. pylori antibodies in patients with anti-phospholipid syndrome, giant cell arteritis, SSc and PBC[41]. Such findings have also been reported in the past. Kalabay et al[42] have studied the prevalence of anti-H. pylori antibodies in various autoimmune rheumatic diseases. These authors have found comparable prevalence of this pathogen in patients with SLE and healthy controls (57% vs 59%)[42]. The highest prevalence of anti-H. pylori antibodies was found in patients with undifferentiated connective tissue disorders (82%)[42]. Of interest, an early study reported a negative association between H. pylori seropositivity and the development of SLE in African-American women[43]. In particular, female African-American patients with SLE had a lower prevalence of H. pylori seropositivity compared to controls (38.1% vs 60.2%). That study also found that seronegative African-American females were more likely to develop SLE, and at an earlier age than their seropositive counterparts[43]. Thus, the mean age of onset for SLE was 34.4 years in the seropositive group and 28 years in the seronegative group. These data suggest that either the presence of the pathogen confers protection from SLE or that the same mechanisms that make individuals prone to H. pylori infection also promote the immune dysregulation which is necessary for SLE’s induction in African-American females.

Much like RA, the role of H. pylori in SLE is also inconclusive. In an animal model, urease exposure induced anti-ssDNA antibody production[22]. However, low anti-H. pylori antibodies have been found in SLE patients, with levels comparable to healthy controls[27,43]. Overall, the evidence does not support a role for H. pylori in the development of SLE[44].

Systemic sclerosis

Dysregulation of innate and adaptive (humoral and cellular) immunity plays an important role in the induction of SSc[45-47]. The very low concordance rate for SSc in monozygotic twins has led investigators to consider that the pathogenesis of this disease rests more in the effect of environmental factors (including viruses and bacteria) rather than genetic influences[48].

In a Japanese cohort of SSc patients, IgG antibodies against H. pylori were found in 55.6% of the patients, a prevalence significantly higher compared to that in the control group[49]. Another Japanese study found a similar prevalence of these antibodies (57.8%), and also a higher prevalence of reflux esophagitis amongst anti-H. pylori antibody-positive patients compared to anti-H. pylori antibody-negative patients[50]. Others have also noted an increased rate of H. pylori infection in patients with SSc compared to controls[15,23,51,52]. However, a significant number of studies has failed to find an increased prevalence of H. pylori seropositivity compared to control groups, further indicating the lack of conclusive data regarding the extent by which H. pylori confers susceptibility to SSc[53-56].

Of clinical relevance, early data have indicated that H. pylori eradication improves Raynaud’s phenomenon in patients with SSc[57,58]. Another study has noted that skin involvement appears to be a predominant feature of H. pylori-infected SSc patients compared to their seronegative counterparts. No other clinical parameters, including the distribution of sex, age, disease duration, autoantibody profile, estimated pulmonary artery systolic pressure, hemoglobin, ESR, renal and liver function indices were different between H. pylori-infected or non-infected SSc patients[59]. On the other hand, SSc patients with Barrett’s esophagus appear less likely to be H. pylori-positive compared to SSc patients without Barrett’s esophagus (10% vs 42.5%). Such findings have underlined the potential protective role of H. pylori for the development of Barrett’s esophagus[60]. In pathophysiological terms, the results of the data discussed so far could be interpreted as follows: (1) H. pylori-infected patients are more prone to develop SSc; (2) SSc patients are more susceptible to infection by H. pylori, probably due to the disturbed gastrointestinal motility which is a characteristic feature of SSc; and (3) after the development of SSc (probably caused by reasons other than H pylori), infection with the pathogen protects the affected patients from unwanted complications (such as Barrett’s esophagus).

Danese et al[56] have tackled the topic from another corner. While they failed to find a difference in the prevalence of the pathogen between SSc patients and controls, they reported that 90% of the H. pylori-positive SSc patients were infected with the virulent CagA strain compared to just 37% of the non-CagA seropositive controls. Elevated levels of anti-hsp65 (but not of anti-hsp60) H. pylori antibodies have been found in SSc patients compared to controls[42].


Data on the potential link between H. pylori and vasculitides are very limited. For example, we know very little about the role of this pathogen in granulomatosis with polyangiitis (GPA), formerly known as Wegener’s granulomatosis. A serological study has shown that anti-H. pylori antibodies are more prevalent in GPA compared to controls[61]. Such findings may be of biological significance as H. pylori has been considered a potential trigger of vascular inflammation. Thus, the SS1 strain of H. pylori-infected heterozygous low density-lipoprotein receptor (LDLR)+/- apoE apolipoprotein E (apoE)+/- mice develop autoimmune inflammation, platelet activation and atherosclerosis[62]. A role for the pathogen in atherosclerosis and vasculitis has been suggested but there is no general agreement on this issue[63]. A previous report was unable to identify significant differences in the rate of anti-H. pylori antibodies between patients with GPA and control diseases[64]. The study by Lidar et al[61] failed to find any association between anti-H. pylori antibody seropositivity in healthy controls and polyarteritis nodosa, microscopic polyangiitis, eosinophilic granulomatosis with polyangiitis (EGPA), also known as Churg Strauss syndrome, and giant cell arteritis[61].

Another study reported disappearance of antiphospholipid syndrome after H. pylori eradication[65], but data are too limited on the issue to draw any conclusions.


H. pylori infection has been considered a potential inducer of several immune-mediated skin disorders. These disorders can be manifestations of systemic vasculitides (Behçet’s disease) or may be related to skin disorders with presumed autoimmune origin (psoriasis, alopecia areata, lichen planus, etc.). Due to space constraints, this review will discuss the role of H. pylori in selected skin disorders including psoriasis, alopecia areata and Behçet’s disease. Other skin disorders linked to H. pylori include, amongst others, atopic dermatitis, chronic or nodular prurigo, recurrent aphthous stomatitis, rosacea, chronic urticaria, lichen planus, and Sweet’s syndrome, and are reviewed elsewhere[66]. We will also discuss the link between H. pylori and chronic urticaria, as a plethora of data have been obtained and the outcomes of these studies are extremely helpful for the understanding of the interactions between the pathogen and the host.


Psoriasis affects 1%-3% of Caucasians. The etiology of the disease remains poorly understood, although immune-mediated mechanisms appear to play a significant role in the development of the disease, including exposure to particular pathogens.

To this end, several studies have investigated a possible link between H. pylori and psoriasis[67-74].

Anti-H. pylori antibodies have been reported to be more prevalent in psoriatic patients compared to controls. For example, Qayoom et al[72] have reported that 40% of psoriatic patients and only 10% of healthy controls (all without known upper gastrointestinal symptoms) had anti-H. pylori antibodies. However, other studies have failed to find any difference in the prevalence of H. pylori[70].

A large study from Turkey, investigating 300 psoriatic patients and 150 controls, has reported comparable prevalence of H. pylori infection in patients and controls. However, the same study suggested that H. pylori status relates to clinical parameters[75], as it was able to show that patients lacking H. pylori had less severe psoriatic disease compared to the seropositive cases. Also, all patients with moderate or severe psoriasis were H. pylori-positive. Intriguingly, patients treated for both psoriasis (with acitretin) and for H. pylori (eradication therapy) showed more rapid improvement of the skin disease, compared to those treated with acitretin only. Notably, psoriasis was also improved in patients receiving only eradication treatment[75]. This study confirmed anecdotal reports or case studies showing that eradication therapy improves psoriasis[73,76].

Strains of H. pylori that express the cytotoxin-associated gene A (CagA) have been associated with a more virulent disease and are believed to play an important role in the clinical outcome of the infection. Several authors have considered that links between the pathogen and autoimmunity may differ in accordance to the virulence of the infecting strain. This has also been the case for H. pylori and psoriasis. To this end, Daudén et al[68] were unable to find any difference in terms of CagA seropositivity between psoriatic patients and patients with non-ulcer dysplasia (54.5% vs 68.1%, respectively).

Chronic urticaria

The pathogenic role of H. pylori infection has been extensively studied in chronic urticaria. Though this disease cannot be considered a typical autoimmune disease, it is of interest to discuss the findings provided so far, as these may help us understand the role of this pathogen in the development of immune-mediated pathologies. Investigations have not been limited to the prevalence of infection[66], but have been extended to include the role of eradication therapy in the clinical course of chronic urticaria[77-86]. Selected papers give us an insight into the extent by which the pathogen and its eradication influence the clinical outcome of the disease. For example, recurrence of urticaria following re-infection by H. pylori has been reported[87]. On the other hand, chronic urticaria has also been described upon administration of eradication therapy for H. pylori infection[79]. Nevertheless, some patients with chronic spontaneous urticaria are resistant to conventional doses of antihistamine medications. A subgroup of those (approximately 28%) receiving both eradication therapy and antihistamines show significant decrease of the Urticaria Activity Score and complete loss of their urticaria symptoms, suggesting that treatment for H. pylori makes these patients less resistant to antihistamines[77]. These findings are in agreement with other studies reporting an overall improvement of chronic urticaria following administration of eradication therapy for H. pylori[88-90]. Other studies have failed to find any relationship between eradication therapy and clinical phenotypes[91]. Of interest, a recent comprehensive review utilized the Grading of Recommendations Assessment, Development, and Evaluation approach to analyze and determine the quality of evidence for this proposed therapy. Their analysis has included 10 trials showing a benefit and 9 trials failing to report a benefit of H. pylori eradication therapy. This analysis reached the conclusion that the evidence provided so far that H. pylori eradication leads to improvement of chronic urticaria outcomes is weak and conflicting. Negative studies showing no benefit in the course of chronic urticaria also led to an overall very low grade of confidence. H. pylori virulent genotypes in the urticaria patients do not appear to affect the clinical course of the disease[92].

Behçet’s disease

The role of H. pylori infection in Behçet’s disease (BeD) remains controversial[93-95]. Most studies originate from Turkey, a country with a high incidence of BeD. Avci et al[95] have failed to find an association between H. pylori and BeD. Other studies published in the form of abstracts or in Turkish journals have published inconsistent results reporting comparable or higher prevalence rates of H. pylori infection in patients with BeD[93]. One study also from Turkey reported an increased seropositivity of H. pylori cytotoxin-associated gene-A in patients with BeD[96].

Improvement of BeD features in patients receiving eradication therapy has also been reported[95], and includes improvements in the cutaneous lesions, arthritis/arthralgia and oral or genital ulcers. The limited number of studies prevents safe conclusions as to the potential links.

Alopecia areata

AA is an immune-mediated disorder characterized by hair loss. The disease affects all ethnic groups, ages, and both sexes. Attempts to investigate the role of H. pylori in this disease have been very few and led to inconclusive results[97,98]. Seroprevalence rates of H. pylori infection in patients with AA are increased or not compared to controls[97,99]. Eradication of H. pylori in AA has also been proposed[100], but not studied extensively.


ITP may occur by itself (idiopathically) or secondary to another condition, including autoimmune conditions (namely AiTD, SLE, anti-phospholipid syndrome). Although the prevalence of H. pylori in ITP patients has been found to be similar to controls[101], improvements in platelet counts following H. pylori eradication have been reported[102-107]. Suzuki et al[106] reported that the platelet response was more pronounced in those patients with the CagA-positive H. pylori strain. Interestingly, anti-CagA antibodies cross-react with peptides expressed on platelets of ITP patients[108]. These findings have led to the suggestion of eradication of H. pylori for the treatment of ITP[109]. Takahashi et al[110] reported that platelet-associated IgG declined after H. pylori eradication, as did molecular mimicry with the CagA region. In that study, H. pylori was found in 75% (15 of 20 patients) of ITP patients of Japanese descent, and eradicated in 87% (13 of 15)[110]. Increased platelet count was observed in 54% (7 of 13) of patients within four months of eradication[110]. Over a dozen other studies have also indicated an improvement in platelet count following H. pylori eradication, and are well-reviewed by Hernando-Harder and colleagues[66]. Platelet eluates from 12 ITP patients recognized H. pylori CagA, although it should be noted that three of the 12 patients were seronegative for H. pylori infection[110]. Levels of anti-CagA antibodies declined in three patients following H. pylori eradication. This latter result suggested a role for cross-reactivity and molecular mimicry[110].

The role of molecular mimicry and cross reactivity between H. pylori components and self-peptides is not new, as antibodies against the H/K-ATPase in the gastric mucosa have been found to be generated via molecular mimicry with H. pylori in atrophic gastritis[111]. Molecular mimicry has been considered a mechanism that could explain other H. pylori-induced autoimmune phenomena, but very few studies have addressed this in an experimental way. The role of CagA strains is also under investigation in other conditions[112,113].


A larger amount of data links H. pylori infection with AiTD, and in particular with Graves’ disease[114]. Bassi and colleagues[115] aimed to correlate the CagA strain of H. pylori with AiTD by investigating 112 consecutive patients at first diagnosis of AiTD. Those researchers tested for H. pylori in stool samples (to confirm ongoing infection), and CagA in serum samples. H. pylori and Graves’ disease were associated (83.7% patients were H. pylori seropositive). No association was found with Hashimoto’s thyroiditis[115]. Most patients (89.2%) seropositive for H. pylori were infected with the CagA strain[115]. This was in accordance with a previous study by the same group[116]. Negative findings in regard to Hashimoto’s were reported in other studies[103,117], while some reported a positive association[114,118,119].

Cross-reactivity between bacterial and thyroid antigens has been proposed as a mechanism in H. pylori-induced AiTD[120]. Indeed, amino acid sequence similarities between CagA H. pylori and thyroid peroxidase have been reported[121], and one group described a reduction in thyroid autoantibodies following H. pylori eradication[122]. Larizza et al[123] suggests that H. pylori may induce or worsen Graves’ disease in patients carrying HLA-DRB10301, and further suggested eradication in certain risk groups. These findings do suggest a possible causative link between the CagA strain of H. pylori and the development of Graves’ disease, but deserve further research. It should be noted that AiTDs are often found concomitantly with other autoimmune conditions, and that the link between the pathogen and autoimmune thyroiditis may indeed reflect a potential contribution of H. pylori in the simultaneous induction of multiple autoimmune diseases in susceptible individuals[124]. The exact mechanisms by which exposure to a microbe elicit more than one autoimmune manifestations are not well defined but cross-reactive responses against a microbial mimic and several self-antigens have been documented[125-127], and may account for this. The reverse is also possible, whereby an autoepitope is cross-reactively targeted by several unrelated microbial mimics in a “multiple hit” scenario[128,129].


H. pylori infection has been considered the likely trigger of various neurological disorders of the central nervous system including MS/NMO, Alzheimer’s disease, Parkinson’s disease, seizure disorders, cerebrovascular diseases, mild cognitive impairment, migraine and ophthalmic disorders, as reviewed elsewhere[130]. A large amount of data has been reported regarding H. pylori and MS/NMO. A recent study by Long et al[131] determined H. pylori infection status in a cohort of 2 NMO patients, 17 at high risk of NMO, 42 MS and 27 healthy controls. H. pylori antibodies were found in 90.4% NMO, 95.8% high-risk NMO, 73.8% MS, and 59.3% controls[131]. There was no statistically significant difference between the MS and control group (P = 0.726)[131]. Interestingly, 93% of patients with aquaporin-4 antibodies were also seropositive for H. pylori[131]. Yoshimura et al[132] analyzed 116 NMO patients for various antibodies to infectious agents, as well as for seropositivity for aquaporin-4 antibodies. They found that H. pylori infection was associated with anti-aquaporin-4 antibody positivity[132]. Similar findings were also reported in other studies[133-135].

Several studies found a lower prevalence of H. pylori amongst MS patients compared to controls. Mohebi and colleagues noted a lower prevalence of H. pylori in a cohort of MS patients[136], in a study which analyzed 163 MS patients and 150 controls for anti-H. pylori IgG and IgM. Seropositive H. pylori patients had a lower MS incidence and fewer neurological complications[136]. Wender also noted a lower anti-H. pylori prevalence in MS vs controls[137]. Li et al[138] evaluated 105 MS patients and 85 controls for antibodies against H. pylori in sera. The MS group was sub-divided into 52 opticospinal MS and 53 conventional MS. In the conventional MS group, 22.6% of patients were positive for anti-H. pylori, compared to 51.9% of opticospinal MS and 42.4% of controls[138]. These data suggest a potential link between NMO and H. pylori, although this does not appear to be the case in MS.


Some Helicobacter species, including H. hepaticus, H. pullorum and H. billis, are more bile-tolerant compared to H. pylori, and can survive in very low concentrations in human bile[139]. This finding has prompted investigators to consider that Helicobacter species other than H. pylori are potential inducers of hepatocyte and biliary epithelia cell autoimmunity. Nevertheless, studies have addressed the role of H. pylori in autoimmune liver diseases, and provided interesting data.

The role of H. pylori has been studied mainly in PBC, an autoimmune cholestatic liver disease characterized by the immune-mediated destruction of small intrahepatic bile ducts. Some studies have also been conducted in PSC, another autoimmune cholestatic disease affecting the larger bile ducts. Studies on the role of this pathogen in the induction of AIH, an autoimmune liver disease affecting hepatocytes, are very limited.

Primary Biliary Cirrhosis

Tanaka et al[140] have failed to detect H. pylori in liver tissues from patients with PBC. Others have been able to detect H. pylori in PBC livers, although this was in a minority of samples tested[140].

Researchers have assessed the seroprevalence of H. pylori in PBC and identified significant differences amongst patients and controls[15]. For example, Shapira et al[41] reported anti-H. pylori antibodies in 54% of patients with PBC compared to 31% (P < 0.01) of patients with other conditions, while Tanaka et al[140] have failed to find any differences between patients and demographically-matched controls (51% vs 46%, respectively).

Our group has assessed the role of molecular mimicry between H. pylori and PBC-specific autoantigens and identified through database searches a significant amino acid sequence similarity between the major mitochondrial autoepitopic region from pyruvate dehydrogenase complex E2 subunit and urease beta of H. pylori[141]. However, we have failed to find any evidence of immunological cross-reactivity at the B-cell level[141]. We also tested the identified mimics as targets of CD4 T-cell responses, and we did not find any significant T-cell recognition[142]. In a subsequent study, we investigated the potential role of cross-reactive antibodies against H. pylori VacA antigen and human PDC-E2, but the results were also negative, clearly demonstrating that these two H. pylori antigens are unlikely candidates as cross-reactive targets in molecular mimicry mechanisms involved in PBC[143].

Primary Sclerosing Cholangitis

An early study in Scandinavian PSC patients indicated detectable H. pylori DNA in livers from patients with PSC and other liver diseases[140]. This has promoted a series of subsequent studies investigating the role of Helicobacter species in PSC and other autoimmune liver diseases. Krasinskas et al[144] detected Helicobacter DNA in 9 of 56 (16%) PSC patients by 16SrRNA PCR, including 7 (12.5% of the total), in whom there was evidence of H. pylori CagA by PCR. Recent PCR analyses have indicated that H. pylori or other Helicobacter species can be detected in up to 13% of liver tissue specimens from pediatric patients with autoimmune sclerosing cholangitis (an autoimmune form of PSC firstly noted in children) and AIH[145]. The same authors detected in the past H. pylori (but not other Helicobacter species) in liver tissues from PBC and adult PSC patients[140].

As PSC patients frequently suffer from ulcerative colitis, it has been hypothesized that alteration in the gut flora due to UC-related intestinal inflammation may promote gut translocation of Helicobacter to the liver. Gut translocation of pathogens appears an attractive mechanism for the induction of liver autoimmunity and there are some data in support of its validity[146,147].

The prevalence of anti-H. pylori antibodies does not differ between pediatric PSC patients (6.6%) and controls (4%-10% depending on the age)[145]. In fact, an increased prevalence of antibodies against non-gastric anti-H. pylori antibodies has been noted in patients with autoimmune liver diseases[148].

Autoimmune Hepatitis

The prevalence of anti-H. pylori antibodies does not appear to differ between patients with AIH (pediatric or adult) and controls[149-151]. Also, H. pylori DNA can be found in a minority of liver tissue samples from patients with AIH with no difference between patients and controls. Currently, there is insufficient evidence to link H. pylori with AIH.


The role of infectious agents in the development of autoimmune disease has been studied extensively. H. pylori is included among those organisms that have been investigated, although findings vary from one condition to the next. Large amounts of data suggest a plausible link with AiTD, NMO, ITP and psoriasis. Less evidence is present regarding RA, SLE, BeD, PBC, AIH and MS. There is inconclusive evidence regarding SjS, SSc, PSC and AA. Table 3 gives an overview of the major findings in support or against the implication of H. pylori in the development of these diseases.

Table 3 Evidence in support or against the role of Helicobacter pylori in autoimmune disease.
Autoimmune conditionEvidence in support and/or against the role of H. pyloriOverall opinion
Oral cavity populated with H. pylori
Higher level of anti-H. pylori antibodies in SjS patients
Increased incidence of mucosal associated lymphoid tissue and lymphomas in parotid and lacrimal glands of SjS patients
Low levels of anti-H. pylori antibodies in SjS patients compared to controls
Higher incidence of H. pylori antibodies in SSc patients than controls
H. pylori eradication improves Raynaud's in SSc patients
Possible protective role against Barrett's esophagus
Higher level of CagA strain H. pylori infected patients
Low incidence of anti-H. pylori antibodies compared to controls
Increased rheumatoid factor IgM from B cells chronically stimulated with H. pylori urease
Low prevalence of anti-H. pylori in RA patients
Unchanged clinical course or symptomatology after H. pylori eradication
H. pylori urease exposure induced anti-ssDNA antibody production in an animal model of SLE
Low levels of anti-H. pylori found among SLE patients, at levels comparable to controls
Negative association between H. pylori seropositivity and the development of SLE in African-American women
Improvement of platelet counts following H. pylori eradication (CagA type H. pylori in particular)
Anti-CagA antibodies cross-react with peptides on platelets of ITP patient
Platelet associated IgGs declined following H. pylori eradication
Found in high prevalence in some ITP cohorts
Platelet eluates from ITP patients recognize H. pylori CagA
Low levels of H. pylori found in ITP patients
AiTDSupport:Probable in Graves’ disease
Higher seropositivity and positive stool cultures for H. pylori in Graves’ disease patients
CagA strain predominant among Graves’ disease patients
Amino acid similarities between CagA and thyroid peroxidase
Reduction in anti-thyroid antibodies following H. pylori eradication
Against:Unlikely in Hashimoto’s thyroiditis
Low levels of infection among Hashimoto’s thyroiditis patients
MS and NMOSupport:Probable in NMO
High rate of H. pylori infection among NMO patients
Correlation between H. pylori infection and presence of aquaporin-4 antibodies
Against:Unlikely in MS
H. pylori infection rates in MS patients similar to or lower than control groups
Higher levels of anti-H. pylori antibodies in patients
Appears to be correlation between H. pylori infection and disease severity
Clinical improvement following H. pylori eradication
No difference in anti-H. pylori levels compared to controls
No difference of CagA seropositivity between patients and controls
Behçet’s diseaseSupport:Unlikely
Higher infection prevalence in patients
Some clinical improvement noted after eradication
No difference between patients and controls
Alopecia areataSupport:Unlikely
Higher infection prevalence
No difference in infection prevalence between patients and controls
Higher prevalence of anti-H. pylori antibodies among PBC patients
Amino acid similarities between pyruvate dehydrogenase E2 (PDC-E2) and urease beta of H. pylori
No differences of infection found between patients and controls
No immunological cross reactivities at the B or CD4 T-cell level
No crossreactivity between H. pylori VacA and PDC-E2
No current evidence
No differences in anti-H. pylori antibodies between patients and controls
No significant difference between H. pylori in liver tissues in patients compared to controls
Detectable H. pylori DNA in PSC liver samples
CagA in samples from PSC patients
Concomitant ulcerative colitis may be related to H. pylori translocation from the gut to the liver
No difference in H. pylori prevalence among pediatric or adult PSC patients compared to controls
No significant difference between H. pylori in liver tissues in patients compared to controls

Idiopathic diseases with an autoimmune component have been the focus of investigation in regard to the role of H. pylori. For example, an autoimmune form of idiopathic dysrhythmias has been linked specifically with CagA and VacA-positive H. pylori strains[152]. This indicated the potential of the pathogen to be linked with conditions now considered “idiopathic”. Also, parasitic diseases such as the Trypanosma cruzi-induced Chagas disease need to be revisited, especially under recent developments showing not only that a proportion of these patients present with autoimmune features but also because such patients are also co-infected with H. pylori strains[153]. In addition, other conditions that are now considered to be autoimmune (such as chronic fatigue syndrome) have not been evaluated for H. pylori involvement.

H. pylori is one of the very few infectious agents (along, for example, with Epstein-Barr virus) that have been considered a common denominator in more than 30 autoimmune disorders (Figure 1). Most research in this area has been limited to serological studies investigating two main topics: first, the prevalence of H. pylori in the disease under investigation vs the control groups; and second, the extent by which H. pylori eradication improves the symptomatology of the patients. However, both approaches suffer from conceptual and design constraints. For example, serological studies investigating the prevalence of anti-H. pylori antibodies in patients and controls have so far provided discrepancies. Demographic details which are known to affect H. pylori status must also be taken into account in cohort selection. This approach will help us to understand whether H. pylori infection predisposes to (or protects from) the development of specific autoimmune diseases. Also, the fact that the prevalence of H. pylori infection does not differ amongst diseases and control groups does not necessarily mean that this pathogen does not play an important role in the development of immune-mediated disease. Thus, several investigators have considered that it is not the infection per se but the ability of susceptible individuals to mount an immune response against hsps or other immunologically-important H. pylori antigens that plays a permissive role in the loss of immunological tolerance to self-antigens. A possibility also exists that the pathogen exerts its pathogenic effects in a “hit-a-run” scenario, (i.e., long after the inflammation caused by the original infection). This could make it almost impossible to link the disease with the microbe in biological material from individuals already suffering from the disease and its unwanted complications. Longitudinal studies enrolling patients at very early stages of the disease may help us to address this issue. For example, relevant autoantibodies may appear years before clinical manifestations of RA or SLE present. Researchers must also take into account reports indicating that infection with this pathogen may indeed confer protection rather than susceptibility to the development of autoimmunity.

Figure 1
Figure 1 A “multiple hit” molecular mimicry mechanism involving microbial mimics originated from Helicobacter pylori and other microbes linked with primary biliary cirrhosis. The major autoepitope of primary biliary cirrhosis-specific anti-mitochondrial antibodies (PDC-E2, pyruvate dehydrogenase complex) shares amino acid similarities with 4 microbial mimics from Helicobacter pylori (H. pylori)[142], N. aromaticivorans[154], L. delbrueckii[155,156], and E. coli[140,157,158]. The working hypothesis is that exposure of susceptible individuals to infections caused by these microbial agents will initiate humoral and cellular immune responses against microbial epitopes (in our case, these will be those sharing similarity with the self-epitope). Antibodies or T-cells against the microbial mimics may then cross-react with the human autoepitope initiating an autoreactive immune response which could lead to the induction of cellular damage and the perpetuation of autoimmunity (and can cause autoimmune disease). Experimental data so far provided demonstrate the existence of cross-reactive responses between self and microbial peptides from E. coli, N. amoraticivorans, and L. delbrueckii. However, experimental testing has shown that the H. pylori mimic (from urease beta) is not a target of cross-reactive responses specifically present in primary biliary cirrhosis[159]. The prevailing notion is that the mimic from H. pylori does not share amino acid similarity to an extent that could initiate cross-reactive response. On the contrary, the other microbial mimics have sufficient homologies with the human autoepitope and can promote molecular mimicry-based immune responses against self.

Another topic which needs to be addressed is that the eradication of other autoimmune disease-relevant microbial agents is responsible for the improvement of symptoms of the patients receiving eradication therapy for H. pylori. In addition, H. pylori eradication may alter the microbiome status of the infected individuals, possibly promoting the persistence of potent infectious inducers of autoimmunity[5]. An immunosuppressive effect of medication may be another possibility. These hypotheses need to be addressed experimentally. Also, work on animal models of diseases and the role of infection with this pathogen are scarce. It is therefore apparent that the role of H. pylori in the development of autoimmune disease needs further research, as positive findings may indicate the need for eradication of the pathogen to alter the clinical course, or prevent autoimmune disease in those at risk.

In conclusion, H. pylori remains one of the most attractive candidate pathogens that could trigger autoimmunity. The ubiquitous nature of this pathogen may explain why it has been implicated in a large number of autoimmune conditions. There is no doubt that more basic work in immunological aspects of the microbial-host interactions is needed to address the pathogenic role of this multi-faceted pathogen.


P- Reviewers: Jelavic B, Xu WX S- Editor: Qi Y L- Editor: Logan S E- Editor: Liu XM

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