清道夫受体CD36在减压病小鼠模型中微粒介导的神经炎症中的关键作用。

IF 3.3 3区 医学 Q1 PHYSIOLOGY
Abid R Bhat, Awadhesh K Arya, Zuha Imtiyaz, Su Xu, Stephen R Thom
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引用次数: 0

摘要

血源性微粒(MPs)在多种形式的脑损伤中发挥作用,但它们如何与脉管系统相互作用并导致神经炎症尚不清楚。清道夫受体CD36在各种细胞类型中表达,并调节炎症、血管功能和先天免疫。我们假设CD36在减压病(DCS)小鼠模型中介导MPs诱导的神经炎症反应。经减压的野生型小鼠和naïve小鼠注射减压小鼠的MPs后,血管周围MPs沉积升高2.2±0.5倍,血液中炎症MPs升高2.8±0.6倍,颈部淋巴结炎症MPs升高2.4±0.4倍,中性粒细胞活化增加2.7±0.6倍,淋巴流量增加2.0±0.3倍,血脑屏障6兆达尔顿右糖酐渗漏增加3.1±0.4倍,脑内炎症蛋白增加一倍。这些事件在CD36敲除小鼠和内皮细胞CD36条件缺陷小鼠(FLOX)中没有发生。我们得出结论,炎症性MPs与内皮细胞CD36相互作用介导DCS的神经炎症反应和血管损伤。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Critical role for scavenger receptor CD36 in microparticle-mediated neuroinflammation in a murine model of decompression sickness.

Blood-borne microparticles (MPs) play a role in several forms of brain injury, but how they interact with the vasculature and contribute to neuroinflammation is unknown. The scavenger receptor CD36 is expressed across various cell types and regulates inflammation, vascular function, and innate immunity. We hypothesized that CD36 mediates MPs induced neuroinflammatory responses in a murine model of decompression sickness (DCS). Wild type mice subjected to decompression and naïve mice injected with MPs from decompressed mice exhibited a 2.2±0.5 fold elevation in perivascular MPs deposition, 2.8 ±0.6 fold elevation of inflammatory MPs in blood and 2.4 ±0.4 fold in cervical lymph nodes, 2.7 ± 0.6 fold increase in neutrophil activation, 2.0 ± 0.3-fold increased glymphatic flow, 3.1 ± 0.4 fold increased leakage of 6 megadalton dextran at the blood-brain barrier, and a doubling of inflammatory proteins in brain. These events failed to occur in CD36 knock-out mice and those conditionally deficient in endothelial CD36 (FLOX). We conclude that inflammatory MPs interact with endothelial CD36 to mediate neuroinflammatory responses and vascular injury in DCS.

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来源期刊
CiteScore
6.00
自引率
9.10%
发文量
296
审稿时长
2-4 weeks
期刊介绍: The Journal of Applied Physiology publishes the highest quality original research and reviews that examine novel adaptive and integrative physiological mechanisms in humans and animals that advance the field. The journal encourages the submission of manuscripts that examine the acute and adaptive responses of various organs, tissues, cells and/or molecular pathways to environmental, physiological and/or pathophysiological stressors. As an applied physiology journal, topics of interest are not limited to a particular organ system. The journal, therefore, considers a wide array of integrative and translational research topics examining the mechanisms involved in disease processes and mitigation strategies, as well as the promotion of health and well-being throughout the lifespan. Priority is given to manuscripts that provide mechanistic insight deemed to exert an impact on the field.
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