创伤性脑损伤后小胶质细胞的兼职工作：衰老和干扰素影响慢性小胶质细胞反应性。
Microglia moonlighting after traumatic brain injury: aging and interferons influence chronic microglia reactivity.
机构信息
Department of Neuroscience, The Ohio State University Wexner Medical Center, 333 W 10th Ave, Columbus, OH, USA.
Department of Neuroscience, The Ohio State University Wexner Medical Center, 333 W 10th Ave, Columbus, OH, USA; Institute for Behavioral Medicine Research, Ohio State University Wexner Medical Center, 460 Medical Center Drive, Columbus, OH, USA; Chronic Brain Injury Program, The Ohio State University, 190 North Oval Mall, Columbus, OH, USA.
出版信息
Trends Neurosci. 2023 Nov;46(11):926-940. doi: 10.1016/j.tins.2023.08.008. Epub 2023 Sep 16.
Most of the individuals who experience traumatic brain injury (TBI) develop neuropsychiatric and cognitive complications that negatively affect recovery and health span. Activation of multiple inflammatory pathways persists after TBI, but it is unclear how inflammation contributes to long-term behavioral and cognitive deficits. One outcome of TBI is microglial priming and subsequent hyper-reactivity to secondary stressors, injuries, or immune challenges that further augment complications. Additionally, microglia priming with aging contributes to exaggerated glial responses to TBI. One prominent inflammatory pathway, interferon (IFN) signaling, is increased after TBI and may contribute to microglial priming and subsequent reactivity. This review discusses the contributions of microglia to inflammatory processes after TBI, as well as the influence of aging and IFNs on microglia reactivity and chronic inflammation after TBI.
大多数经历创伤性脑损伤 (TBI) 的人会出现神经精神和认知并发症，这会对康复和健康寿命产生负面影响。TBI 后会持续激活多种炎症途径，但尚不清楚炎症如何导致长期的行为和认知缺陷。TBI 的一个后果是小胶质细胞的启动，随后对二次应激源、损伤或免疫挑战产生过度反应，从而进一步加剧并发症。此外，随着年龄的增长，小胶质细胞的启动会导致对 TBI 的神经胶质反应过度。一个突出的炎症途径是干扰素 (IFN) 信号转导，它在 TBI 后增加，并可能导致小胶质细胞的启动和随后的反应性。这篇综述讨论了小胶质细胞对 TBI 后炎症过程的贡献，以及衰老和 IFNs 对 TBI 后小胶质细胞反应性和慢性炎症的影响。
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