Gonciarz Weronika, Matusiak Agnieszka, Rudnicka Karolina, Rechciński Tomasz, Chałubiński Maciej, Czkwianianc Elżbieta, Broncel Marlena, Gajewski Adrian, Chmiela Magdalena
Department of Immunology and Infectious Biology, Institute of Microbiology, Biotechnology and Immunology, Faculty of Biology and Environmental Protection, University of Lodz, Lodz, Poland.
Department of Cardiology Biegański Regional Speciality Hospital, Medical University of Łódź, Łódź, Poland.
APMIS. 2019 Mar;127(3):139-149. doi: 10.1111/apm.12925.
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 C urea breath test ( 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.
幽门螺杆菌（Hp）可能由于分子模拟引发自身免疫反应。本研究旨在比较健康供体（HD）、Hp相关性胃炎患者或冠心病（CHD）患者血清中针对与人Hp热休克蛋白（Hsp）60同源的人热休克蛋白（Hsp）60特定表位（P1肽）的IgG抗体水平。这些患者经快速尿素酶试验、组织学检查（消化不良患者）、¹³C尿素呼气试验（¹³C UBT）确诊有无Hp感染，以及有无抗Hp抗体（健康供体、冠心病患者）。通过用这些细菌吸附血清以及用Hp对豚鼠进行实验性免疫，验证了Hp诱导的抗P1 IgG。还评估了THP-1Blue™单核细胞对P1的细胞因子分泌情况。在感染Hp的胃炎或冠心病患者中检测到抗P1抗体，而在未感染个体或无症状携带者中未发现。任何组中均未检测到针对P2的抗体。用Hp吸附后的血清对P1的交叉反应性降低。感染Hp的豚鼠产生了抗P1自身抗体。THP-1XBlue™单核细胞对P1产生促炎细胞因子反应。Hp阳性的胃炎或冠心病患者中针对P1的自身抗体以及P1对促炎细胞因子的上调可能有助于Hp感染的发病机制。
