Platelets Are Critical Drivers of Illness Behaviors During Liver Inflammation.
Platelets Are Critical Drivers of Illness Behaviors During Liver Inflammation.
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血小板是肝脏炎症期间疾病行为的关键驱动因素。
DOI：
10.1053/j.gastro.2017.09.029
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发表时间：
2017
期刊：
影响因子：
29.4
通讯作者：
Chauhan A
中科院分区：
文献类型：
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作者：
Chauhan A
炎症性疾病通常伴有行为改变或“病态行为”，包括冷漠、社交退缩、疲劳和食欲不振。这些行为可能是作为保护性适应而进化的，以帮助应对疾病的急性期，但如果疾病持续存在，它们可能成为对生活质量产生重大不利影响的主要症状。1，2已经提出，促炎细胞因子的释放激活了最终驱动疾病行为的大脑通信途径，尽管确切的机制仍然知之甚少。3 D 'Mello et al 4在他们的文章“Interactions between platelets and inflammatory monocytes affect sickness behavior in mice with liver inflammation”中，详细描述了血小板在这一过程中的新作用，建立在该小组先前的工作基础上，证明了活化的循环单核细胞如何触发肝脏疾病中炎症诱导的疾病行为。这篇文章是重要的，不仅为机制的见解，它提供了一个鲜为人知的和临床上重要的问题的发病机制，但也因为它有明确的治疗implications.There是证据表明，3种细胞因子肿瘤坏死因子（TNF）-α，白细胞介素（IL）-1b，IL-6-参与疾病行为的免疫学基础。大多数研究都集中在这些细胞因子对大脑的直接影响上，直到Swain小组提出了一种不同的机制来解释这种影响。他们报告说，
Inflammatory diseases are often accompanied by behavioral changes or “sickness behaviors” that include apathy, social withdrawal, fatigue, and loss of appetite. These behaviors have likely evolved as protective adaptations to help deal with the acute phase of illness, but if an illness persists, they can become dominant symptoms exerting major adverse impact on quality of life. 1, 2 It has been proposed that the release of proinflammatory cytokines activates brain communication pathways that ultimately drive sickness behaviors, although the precise mechanisms remain poorly understood. 3 D’Mello et al 4 in their article “Interactions between platelets and inflammatory monocytes affect sickness behavior in mice with liver inflammation,” detail a new role for platelets in this process, building on the previous work from this group demonstrating how activated circulating monocytes can trigger inflammation-induced sickness behaviors in liver disease. This article is important not only for the mechanistic insights it provides to the pathogenesis of a poorly understood and clinically important problem, but also because it has clear therapeutic implications.There is evidence that 3 cytokines—tumor necrosis factor (TNF)-a, interleukin (IL)-1b, and IL-6—are involved in the immunologic basis of sickness behavior. Most research had focused on the direct effects of these cytokines on the brain until the Swain group proposed a different mechanism to explain the effect. They reported in