Helicobacter pylori (Hp) may initiate autoimmunity as a result of molecular mimicry. The aim of this study was to compare the level of IgG antibodies to a specific epitope (P1 peptide) of human heat shock protein (Hsp)60 homologous to Hp Hsp60 (HspB) in the sera of healthy donors (HD), patients with Hp-related gastritis or coronary heart disease (CHD), uninfected or with Hp infection confirmed by rapid urease test, histological examination (dyspeptic patients) the 13 C urea breath test (13 C UBT), and anti-Hp antibodies (healthy donors, CHD patients). The Anti-P1 IgG induction by Hp was verified by adsorption of sera with these bacteria and by experimental immunization of Caviae porcellus with Hp. Cytokine secretion by THP-1Blue™ monocytes in response to P1 was also assessed. Anti-P1 antibodies were detected in patients with gastritis or CHD infected with Hp and they were not found in uninfected individuals or asymptomatic carriers. No antibodies were raised against P2 in any group. Reduced cross-reactivity to P1 was exhibited by sera adsorbed with Hp. Caviae porcellus infected with Hp produced anti-P1 autoantibodies. THP-1XBlue™ monocytes responded to P1 by production of proinflammatory cytokines. Autoantibodies against P1 in Hp-positive patients with gastritis or CHD and upregulation of proinflammatory cytokines by P1 may contribute to the pathogenesis of Hp infection.
Keywords: Helicobacter pylori; Antigenic mimicry; HspB; atherogenesis; gastritis; human Hsp60.
© 2019 APMIS. Published by John Wiley & Sons Ltd.