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抑制整体蛋白VLA-3和四氨酸CD151可以防止中性蛋白介导的内皮损伤

Chelsey Ciambella¹, Hadley Witt, Catherine M Dickinson¹

¹Rhode Island Hospital, Department of Surgery, Division of Surgical Research, Alpert Medical School of Brown University, Providence, Rhode Island.

Shock (Augusta, Ga.)

|May 30, 2024

概括

抑制中性粒细胞非常晚抗原-3 (VLA-3) 和CD151可以保护内皮细胞在败血症期间免受损伤. 准这些分子可能会在严重疾病中保持器官功能.

科学领域:

免疫学免疫学免疫学
细胞生物学细胞生物学
血管生物学血管生物学

背景情况:

对损伤部位的中性粒细胞招募是必不可少的,但在败血症中可能导致血管损伤.
激活的中性粒细胞与内皮细胞相互作用,可能导致严重的血管损伤.
鉴定参与中性粒细胞尿症的分子为严重疾病提供了治疗点.

研究的目的:

测试抑制中性粒细胞非常晚期抗原-3 (VLA-3;α3β1) 和CD151是否能保护内皮功能免受中性粒细胞介导的损伤.
研究VLA-3和CD151在中性粒细胞诱导的内皮功能障碍中的作用.

主要方法:

来自败血症患者和健康捐献者的血液被用于隔离中性粒细胞.
人类带血管内皮细胞被TNF-α激活,并使用电池阻抗传感测量它们的电阻.
在与内皮细胞共同培养之前,中性粒细胞被用阻断VLA-3和/或CD151的抗体治疗.

主要成果:

来自败血症患者或活化ex vivo的中性粒细胞比健康的中性粒细胞造成更大的内皮单层损伤.
对VLA-3和/或CD151的抗体阻断显著减少了中性粒细胞诱导的内皮损伤.
这些保护作用在各种基质 (纤维素,原,拉米宁) 中观察到,表明广泛的组织相关性.

结论:

激活的人类中性粒细胞上非常晚的抗原-3 (VLA-3) 和CD151是内皮损伤的关键媒介.
向VLA-3和CD151可能代表一种治疗策略,以在严重疾病中保持内皮和器官功能.

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