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抗幽门螺杆菌热休克蛋白 60 抗体加重 HSP60 介导的促炎反应。

Antibodies against Helicobacter pylori heat shock protein 60 aggravate HSP60-mediated proinflammatory responses.

机构信息

Department of Biological Science and Technology and Institute of Molecular Medicine and Bioengineering, National Chiao Tung University, Hsinchu, Taiwan.

出版信息

Cytokine. 2011 Aug;55(2):174-80. doi: 10.1016/j.cyto.2011.04.011. Epub 2011 May 11.

DOI:10.1016/j.cyto.2011.04.011
PMID:21565524
Abstract

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-α 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-α 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-α production. The pathogen-specific antibodies may execute potential immune functions rather than recognize or neutralize microbes.

摘要

抗幽门螺杆菌热休克蛋白 60(HpHSP60)抗体通常存在于幽门螺杆菌感染患者中,已知与胃疾病的进展有关。然而,这些抗体对 HpHSP60 功能的影响尚未确定。本研究旨在探讨抗 HSP60 抗体与 HpHSP60 之间的相互作用对炎症反应的影响。制备了抗 HpHSP60 多克隆血清和单克隆抗体(mAbs),以评估它们对 HpHSP60 诱导的 IL-8 和 TNF-α 活性的影响。结果表明,从感染幽门螺杆菌的患者或用 HpHSP60 免疫的兔和小鼠中收集的抗 HpHSP60 多克隆血清可显著增强 HpHSP60 介导的单核细胞 THP-1 细胞中 IL-8 和 TNF-α 的分泌。抗 HpHSP60 mAbs 也发现了类似的效果。进一步分析表明,这种现象仅由抗 HpHSP60 抗体引起,而不是由其他非特异性 mAbs 引起。此外,非特异性 mAbs 降低了 HpHSP60 和抗 HpHSP60 mAbs 在诱导促炎细胞因子中的协同作用。在此,我们首次检查了抗 HpHSP60 抗体在宿主免疫反应中的作用。本研究表明,H. pylori 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制。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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Antibodies against Helicobacter pylori heat shock protein 60 aggravate HSP60-mediated proinflammatory responses.抗幽门螺杆菌热休克蛋白 60 抗体加重 HSP60 介导的促炎反应。
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