Sarnat Harvey B, Scantlebury Morris H
Department of Pediatrics, University of Calgary Cumming School of Medicine and Alberta Children's Hospital Research Institute, Calgary, Alberta, Canada; Department of Pathology and Laboratory Medicine (Neuropathology), University of Calgary Cumming School of Medicine and Alberta Children's Hospital Research Institute, Calgary, Alberta, Canada; Department of Clinical Neurosciences, University of Calgary Cumming School of Medicine and Alberta Children's Hospital Research Institute, Calgary, Alberta, Canada.
Department of Pediatrics, University of Calgary Cumming School of Medicine and Alberta Children's Hospital Research Institute, Calgary, Alberta, Canada; Department of Clinical Neurosciences, University of Calgary Cumming School of Medicine and Alberta Children's Hospital Research Institute, Calgary, Alberta, Canada.
Semin Pediatr Neurol. 2017 Aug;24(3):152-160. doi: 10.1016/j.spen.2017.08.010. Epub 2017 Sep 14.
Though the term "inflammation" is traditionally defined as proliferation or infiltration of lymphatic cells of the lymphatic immune system and macrophages or as immunoreactive proteins including cytokines, interleukins and major histocompatibility complexes, recently recognized reactions to tissue injury also are inflammation, often occurring in the central nervous system in conditions where they previously were not anticipated and where they may play a role in both pathogenesis and repair. We highlight 4 such novel inflammatory conditions revealed by neuropathologic studies: (1) inflammatory markers and cells in the brain of human fetuses with tuberous sclerosis complex and perhaps other disorders of the mechanistic target of rapamycin genetic or metabolic pathway, (2) inflammatory markers in the brain related to febrile seizures of infancy and early childhood, (3) heat-shock protein upregulation in glial cells and neurons at sites of chronic epileptic foci, and (4) the emerging role of astrocytes in the presence of and participation in inflammation. Novel evidence shows that cerebral inflammation plays a role in some genetic diseases as early as midgestation and thus is not always acquired postnatally or in adult life.
尽管“炎症”一词传统上被定义为淋巴免疫系统的淋巴细胞和巨噬细胞的增殖或浸润，或作为包括细胞因子、白细胞介素和主要组织相容性复合体在内的免疫反应性蛋白质，但最近认识到的对组织损伤的反应也是炎症，常在中枢神经系统中发生，而此前在这些情况下并未预期到炎症的存在，并且炎症可能在发病机制和修复过程中都发挥作用。我们着重介绍神经病理学研究揭示的4种此类新型炎症情况：（1）患有结节性硬化症复合体以及可能患有雷帕霉素机制靶点基因或代谢途径其他紊乱疾病的人类胎儿大脑中的炎症标志物和细胞，（2）与婴儿期和幼儿期热性惊厥相关的大脑炎症标志物，（3）慢性癫痫病灶部位的胶质细胞和神经元中热休克蛋白的上调，以及（4）星形胶质细胞在炎症存在和参与过程中所起的新作用。新证据表明，脑炎症早在妊娠中期就在某些遗传疾病中发挥作用，因此并不总是在出生后或成年期才出现。
