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首页> 外文期刊>Cytokine >Antibodies against Helicobacter pylori heat shock protein 60 aggravate HSP60-mediated proinflammatory responses.
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Antibodies against Helicobacter pylori heat shock protein 60 aggravate HSP60-mediated proinflammatory responses.

机译：针对幽门螺杆菌热休克蛋白60的抗体会加重HSP60介导的促炎反应。

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摘要

Anti-Helicobacter pylori heat shock protein 60 (HpHSP60) antibodies are usually found in H. pylori-infected patients and are known to be associated with the progression of gastric diseases. However, the effects of these antibodies on the functions of HpHSP60 have not been identified. This study aims to investigate the effects of the interaction between anti-HSP60 antibodies and HpHSP60 on inflammatory responses. Anti-HpHSP60 polyclonal sera and monoclonal antibodies (mAbs) were produced to evaluate their effects on HpHSP60-induced IL-8 and TNF-alpha activity. The results indicated that anti-HpHSP60 polyclonal sera collected from patients infected with H. pylori or from rabbit and mice immunized with HpHSP60 could significantly enhance HpHSP60-mediated IL-8 and TNF-alpha secretion from monocytic THP-1 cells. Similar effects were also found with anti-HpHSP60 mAbs. Further analysis revealed that this phenomenon was only carried out by anti-HpHSP60 antibody but not by other non-specific mAbs. Moreover, the non-specific mAbs decreased the synergism of HpHSP60 and anti-HpHSP60 mAbs in proinflammatory cytokine induction. Herein, we have examined the role of anti-HpHSP60 antibody in host immune responses for the first time. This study demonstrated that H. pylori HSP60/mAbs could modulate helicobacterial pathogenesis by increasing IL-8 and TNF-alpha production. The pathogen-specific antibodies may execute potential immune functions rather than recognize or neutralize microbes.
机译：抗幽门螺杆菌热休克蛋白60（HpHSP60）抗体通常在幽门螺杆菌感染的患者中发现，并且已知与胃疾病的进展有关。但是，尚未确定这些抗体对HpHSP60功能的影响。这项研究旨在调查抗HSP60抗体和HpHSP60之间的相互作用对炎症反应的影响。产生了抗HpHSP60多克隆血清和单克隆抗体（mAb），以评估它们对HpHSP60诱导的IL-8和TNF-α活性的影响。结果表明，从幽门螺杆菌感染的患者中或从用HpHSP60免疫的兔和小鼠中收集的抗HpHSP60多克隆血清可以显着增强HpHSP60介导的单核细胞THP-1细胞的IL-8和TNF-α分泌。抗HpHSP60 mAb也发现了类似的效果。进一步的分析表明，这种现象仅由抗HpHSP60抗体引起，而没有由其他非特异性mAb引起。而且，非特异性mAb在促炎细胞因子诱导中降低了HpHSP60和抗HpHSP60 mAb的协同作用。在本文中，我们首次检查了抗HpHSP60抗体在宿主免疫反应中的作用。这项研究表明幽门螺杆菌HSP60 / mAbs可以通过增加IL-8和TNF-α的产生来调节幽门螺杆菌的发病机理。病原体特异性抗体可能执行潜在的免疫功能，而不是识别或中和微生物。

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