Abstract

Infectious diseases, such as Helicobacter pylori, which produce systemic inflammation may be one key factor in the onset of autoimmunity. The association between H. pylori and antinuclear antibodies (ANA), a marker of autoimmunity, has been understudied. Data from the 1999-2000 National Health and Nutrition Examination Survey were used to evaluate the cross-sectional association between H. pylori seroprevalence and ANA positivity in US adults aged ≥20 years. ANA was measured in a 1:80 dilution of sera by indirect immunofluorescence using HEp-2 cells (positive ⩾3). H. pylori immunoglobulin G enzyme-linked immunosorbent assays were used to categorise individuals as seropositive or seronegative. H. pylori seropositivity and ANA positivity were common in the adult US population, with estimated prevalences of 33.3% and 9.9%, respectively. Both were associated with increasing age. H. pylori seropositivity was associated with higher odds of ANA (prevalence odds ratio = 1.89, 95% confidence interval = 1.08-3.33), adjusted for age, sex, race/ethnicity, educational attainment and body mass index. H. pylori infection may be one key factor in the loss of self-tolerance, contributing to immune dysfunction.

Highlights

  • Loss of self-tolerance is a hallmark of autoimmune disease, but less well understood are the drivers of self-tolerance loss in the immune system

  • Using data from the 1999–2000 National Health and Nutrition Examination Survey (NHANES), we evaluated the crosssectional association between H. pylori seroprevalence and Antinuclear antibodies (ANA) positivity in the adult US population

  • P-valuea 0.59 0.004

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Summary

Introduction

Loss of self-tolerance is a hallmark of autoimmune disease, but less well understood are the drivers of self-tolerance loss in the immune system. Antinuclear antibodies (ANA), representing humoral immunity to cellular components, are one indicator of autoimmunity that occurs in the context of the failure of self-tolerance mechanisms. Infectious agents may be important environmental exposures resulting in autoimmunity. Chronic infections that have evolved extensive immune evasion mechanisms are of interest as potential drivers of self-tolerance loss. One such infectious agent is Helicobacter pylori, a bacterium often contracted in childhood, which colonises the mucosal layer of the gastric epithelium [3]. H. pylori infection is common, with the prevalence being approximately 50% worldwide [5, 6], and is well-known for its causative role in gastritis and peptic ulcer disease [7]. H. pylori infection may remain for many years, if not the entire life of the individual, as the infection is often asymptomatic [7]

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