Gonciarz Weronika, Tomaszewska Agata, Krupa Agnieszka, Rechciński Tomasz, Chałubiński Maciej, Broncel Marlena, Chmiela Magdalena
Department of Immunology and Infectious Biology, Institute of Microbiology, Biotechnology and Immunology, Faculty of Biology and Environmental Protection, University of Łódź, Banacha 12-16, 90-237 Lodz, Poland.
Lodz Institutes of the Polish Academy of Sciences, The Bio-Med-Chem Doctoral School, University of Lodz, Banacha 12/16, 90-237 Lodz, Poland.
J Clin Med. 2022 May 1;11(9):2545. doi: 10.3390/jcm11092545.
Molecular mimicry between (Hp) and the host components resulting in induction of cross-reacting antibodies has been suggested as accessory mechanism in the development of coronary heart disease (CHD). A potential target for antibodies induced during Hp infection by the components of these bacteria might be amino acid sequence TVLLPVIFF (P1) of tumor necrosis factor receptor (TNFR), which is exposed on vascular endothelium and immunocompetent cells, driving inflammation.
To examine whether anti-P1 IgG are induced during Hp infection in CHD patients.
Sera from CHD patients infected with Hp (54) vs. sera of uninfected healthy donors (22) were tested by the ELISA for anti- antibodies, anti-P1 IgG, and for antibodies towards control sequence IAKEGFEKIS (P2). Sera of infected experimentally with Hp (30) or uninfected (10) were included into this study. The same serum samples, which were positive for anti-P1 IgG, were adsorbed with Hp and then subjected to the ELISA. The biological activity of anti-P1 IgG was assessed in complement (C1q) binding assay.
Sera of 43 CHD patients seropositive for anti-Hp IgG contained anti-P1 IgG binding C1q. Additionally, 10 serum samples of animals seropositive for anti-Hp IgG contained anti-P1 IgG. Anti-P1 IgG in tested sera were neutralized by their adsorption with Hp.
In CHD patients infected with Hp, antibodies cross-reacting with TNFR common sequence are produced. Further studies are necessary to define immunogenic Hp determinants and to confirm possible cellular effects of cross-reacting antibodies.
幽门螺杆菌（Hp）与宿主成分之间的分子模拟导致交叉反应性抗体的诱导，这被认为是冠心病（CHD）发生发展的辅助机制。这些细菌成分在Hp感染期间诱导产生的抗体的一个潜在靶标可能是肿瘤坏死因子受体（TNFR）的氨基酸序列TVLLPVIFF（P1），该序列暴露于血管内皮和免疫活性细胞上，可引发炎症。
检测冠心病患者Hp感染期间是否诱导产生抗P1 IgG。
采用酶联免疫吸附测定（ELISA）检测54例感染Hp的冠心病患者血清与22例未感染的健康供者血清中的抗P1抗体、抗P1 IgG以及针对对照序列IAKEGFEKIS（P2）的抗体。本研究纳入了30例经实验感染Hp或10例未感染的动物血清。将抗P1 IgG呈阳性的相同血清样本用Hp吸附，然后进行ELISA检测。通过补体（C1q）结合试验评估抗P1 IgG的生物学活性。
43例抗Hp IgG血清学阳性的冠心病患者血清中含有结合C1q的抗P1 IgG。此外，10例抗Hp IgG血清学阳性的动物血清样本中也含有抗P1 IgG。检测血清中的抗P1 IgG通过用Hp吸附而被中和。
在感染Hp的冠心病患者中，产生了与TNFR共同序列发生交叉反应的抗体。需要进一步研究来确定Hp的免疫原性决定簇，并证实交叉反应性抗体可能的细胞效应。
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