在创伤性脑损伤后的神经心脏炎症轴
Robert W Keane1,2, Roey Hadad2, Xavier O Scott2
1Department of Neurological Surgery and The Miami Project to Cure Paralysis, University of Miami Miller School of Medicine, Miami, FL 33136, USA.
Pharmaceuticals (Basel, Switzerland)
|October 28, 2023
概括
创伤性脑损伤 (TBI) 触发了携带炎症蛋白质的细胞外囊泡 (EV) 的释放. 这些EV激活心脏炎症细胞,导致TBI后的全身炎症和心脏损伤.
科学领域:
- 神经科学是一个神经科学.
- 免疫学 免疫学 免疫学
- 心血管科学 心血管科学
背景情况:
- 创伤性脑损伤 (TBI) 会导致系统性炎症,影响外周器官.
- 将TBI与心脏功能障碍等并发症联系在一起的机制尚未完全理解.
- 炎症酶激活与TBI后的炎症反应有关.
研究的目的:
- 为了调查TBI后是否释放含有炎症蛋白的细胞外囊泡 (EVs).
- 为了确定这些EV是否激活心脏炎症细胞并导致组织损伤.
- 探索EVs在TBI引起的全身炎症中的作用.
主要方法:
- 在C57BL/6小鼠中控制的皮质冲击 (CCI) 模型.
- 在大脑,血清和心脏组织中分析炎症蛋白水平.
- 使用纳米粒子跟踪分析和Ella Simple Plex进行血清衍生EV的表征.
- 质谱测量用于识别EV中的蛋白质.
- 在体外研究EV对心脏细胞的影响.
主要成果:
- 在小鼠的心房和皮层中,TBI增加了炎症酶蛋白 (AIM2,ASC,caspases-1, -8,-11).
- 来自TBI患者的血清衍生的EV显示了高水平的caspase-1,ASC和IL-18.
- 来自TBI患者的EV诱导了心脏细胞中的炎症酶激活.
- 质谱测量确定了TBI衍生的EV中的补充和心血管信号蛋白.
结论:
- 创伤诱导心脏中的炎症酶激活,部分由EVs调解.
- 这些EV携带着炎症和补充蛋白质,有助于全身炎症.
- 在TBI后释放的EV在外周器官损伤中发挥作用,特别是在心脏中.
相关概念视频
Secondary Spinal Cord Injury llI: Pathophysiology
Early Ischemia and Ionic ImbalanceWithin minutes of spinal cord injury, a secondary cascade begins, progressing over hours to weeks. Vascular damage reduces blood flow, causing ischemia and mitochondrial dysfunction. ATP depletion leads to ion pump failure, membrane depolarization, sodium influx, potassium efflux, and water accumulation, resulting in cellular swelling. Increased intracellular calcium further disrupts mitochondria and accelerates cellular injury.Excitotoxicity and Neuronal...
Traumatic Brain Injury l: Introduction
DefinitionTraumatic brain injury, or TBI, is a disturbance of normal brain function induced by an external mechanical force, such as a direct blow to the head or a penetrating injury. It can affect both brain structure and function, producing a wide range of clinical outcomes. TBI is a heterogeneous condition, meaning its effects may differ based on the type, location, and severity of the injury.Basis of ClassificationTBI is classified based on severity, injury mechanism, or pathophysiology. In...
Bacterial Meningitis II: Pathophysiology
Bacterial meningitis typically begins when pathogens such as Neisseria meningitidis and Streptococcus pneumoniae colonize the nasopharynx and invade the bloodstream. This process is facilitated by bacterial virulence factors, such as polysaccharide capsules, which resist phagocytosis and complement-mediated killing. Less commonly, bacteria reach the central nervous system via contiguous spread from infections like otitis media or sinusitis, through congenital or acquired dural defects, or...
Gut-Brain Axis
The gut–brain axis is a bidirectional communication system that connects the gastrointestinal tract and the brain. This interaction is mediated through multiple pathways, including the vagus nerve, hormonal signals, immune responses, and chemical messengers produced by gut microbes.Microbial Contributions to Brain FunctionGut microbiota contributes significantly to brain function by producing neuroactive compounds. These include neuroactive compounds that influence neurotransmitters such as...


