Department of Neuroscience, McKnight Brain Institute, University of Florida, Gainesville (E.C-J).
Biomedical MR Imaging and Spectroscopy Group, Center for Image Sciences, University Medical Center Utrecht, the Netherlands (R.M.D.).
Stroke. 2022 May;53(5):1473-1486. doi: 10.1161/STROKEAHA.122.036946. Epub 2022 Apr 7.
Maintaining blood-brain barrier (BBB) integrity is crucial for the homeostasis of the central nervous system. Structurally comprising the BBB, brain endothelial cells interact with pericytes, astrocytes, neurons, microglia, and perivascular macrophages in the neurovascular unit. Brain ischemia unleashes a profound neuroinflammatory response to remove the damaged tissue and prepare the brain for repair. However, the intense neuroinflammation occurring during the acute phase of stroke is associated with BBB breakdown, neuronal injury, and worse neurological outcomes. Here, we critically discuss the role of neuroinflammation in ischemic stroke pathology, focusing on the BBB and the interactions between central nervous system and peripheral immune responses. We highlight inflammation-driven injury mechanisms in stroke, including oxidative stress, increased MMP (matrix metalloproteinase) production, microglial activation, and infiltration of peripheral immune cells into the ischemic tissue. We provide an updated overview of imaging techniques for in vivo detection of BBB permeability, leukocyte infiltration, microglial activation, and upregulation of cell adhesion molecules following ischemic brain injury. We discuss the possibility of clinical implementation of imaging modalities to assess stroke-associated neuroinflammation with the potential to provide image-guided diagnosis and treatment. We summarize the results from several clinical studies evaluating the efficacy of anti-inflammatory interventions in stroke. Although convincing preclinical evidence suggests that neuroinflammation is a promising target for ischemic stroke, thus far, translating these results into the clinical setting has proved difficult. Due to the dual role of inflammation in the progression of ischemic damage, more research is needed to mechanistically understand when the neuroinflammatory response begins the transition from injury to repair. This could have important implications for ischemic stroke treatment by informing time- and context-specific therapeutic interventions.
维持血脑屏障 (BBB) 的完整性对于中枢神经系统的内稳态至关重要。脑内皮细胞作为 BBB 的结构组成部分,与周细胞、星形胶质细胞、神经元、小胶质细胞和血管周围巨噬细胞相互作用,形成神经血管单元。脑缺血会引发强烈的神经炎症反应,以清除受损组织并为大脑修复做准备。然而,在中风的急性期发生的强烈神经炎症与 BBB 破坏、神经元损伤和更差的神经结局相关。在这里,我们批判性地讨论了神经炎症在缺血性中风病理中的作用,重点关注 BBB 以及中枢神经系统和外周免疫反应之间的相互作用。我们强调了中风中炎症驱动的损伤机制,包括氧化应激、MMP(基质金属蛋白酶)产生增加、小胶质细胞激活和外周免疫细胞浸润到缺血组织。我们提供了一种更新的综述,介绍了用于检测 BBB 通透性、白细胞浸润、小胶质细胞激活和细胞黏附分子上调的体内成像技术,这些变化发生在缺血性脑损伤之后。我们讨论了将成像技术应用于临床以评估与中风相关的神经炎症的可能性,其具有提供图像引导诊断和治疗的潜力。我们总结了几项评估抗炎干预在中风中疗效的临床研究结果。尽管令人信服的临床前证据表明神经炎症是缺血性中风的一个有前途的治疗靶点,但迄今为止,将这些结果转化为临床环境仍然具有挑战性。由于炎症在缺血性损伤进展中的双重作用,需要更多的研究来从机制上理解神经炎症反应何时从损伤转向修复。这对于缺血性中风的治疗具有重要意义,可以告知针对特定时间和特定情况的治疗干预措施。