经过训练的突巨细胞免疫与Staphylococcus aureus感染后的关节炎症和损伤加剧有关
Peter Silva Rocha1, Adryan Aparecido Silva1, Celso Martins Queiroz-Junior2
1Department of Biochemistry and Immunology, Institute of Biological Sciences, Universidade Federal de Minas Gerais, Belo Horizonte, 31270-901, MG, Brazil.
概括
关节炎症在继发性黄金葡萄球菌感染后恶化,这是由于突巨细胞的训练免疫力造成的. 这种免疫反应加剧了关节损伤和疼痛,突出了一个新的治疗点.
科学领域:
- 免疫学 免疫学 免疫学
- 类风湿病学 类风湿病学
- 微生物学 微生物学
背景情况:
- 训练有素的免疫力,是一种天生的免疫记忆,可以影响随后的炎症反应.
- 关节囊里面的细胞 - - 协同细胞 (synoviocytes) 在关节平衡和炎症中起着至关重要的作用.
- 黄金葡萄球菌感染是感染性关节炎的常见原因,导致关节严重损伤.
研究的目的:
- 为了研究是否同胞细胞获得训练有素的免疫特性.
- 为了确定训练有素的免疫力是否会在继发性黄金葡萄球菌感染后加剧关节炎症.
- 为了确定参与这种现象的特定细胞类型和分子通路.
主要方法:
- 小鼠接受了连续的脂多糖 (LPS) 和金黄色葡萄球菌 (Staphylococcus aureus) 的关节内注射.
- 评估了机械感觉,关节炎症和损伤.
- 训练有素的免疫标记物,包括糖分和mTOR通路激活,在突组织和孤立的突细胞中进行了分析.
- 用mTOR抑制剂Rapamycin进行了评估,以评估其治疗潜力.
主要成果:
- 与单次刺激相比,双重LPS-S. aureus刺激导致关节炎症,损伤和持续的恶性感觉增加.
- CX3CR1+突巨细胞显示活性增加和与训练免疫相关的表观遗传修饰,包括mTOR通路上调.
- 拉帕米辛治疗显著减少了巨细胞的激活,关节炎症和骨损伤.
结论:
- 在CX3CR1+突巨体中,表现出训练有素的免疫表型.
- 这种在突巨细胞中训练有素的免疫力有助于恶化关节炎症和败血性关节炎的损伤.
- 准mTOR途径可能提供一种治疗策略,用于管理S. aureus诱导的败血性关节炎.
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