Call Off the Dog(ma): M1/M2 Polarization Is Concurrent following Traumatic Brain Injury.
Call Off the Dog(ma): M1/M2 Polarization Is Concurrent following Traumatic Brain Injury.
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DOI：
10.1371/journal.pone.0148001
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发表时间：
2016
期刊：
影响因子：
3.7
通讯作者：
Rosi S
中科院分区：
文献类型：
--
作者：
Morganti JM;Riparip LK;Rosi S
创伤性脑损伤在原发机械撞击后，可同时产生多种促炎和抗炎分子介质。鉴于细胞类型的多样性及其同源受体的必要表达，这创造了一个高度复杂的炎症环境。在神经创伤的研究中，越来越多的人努力在体外确定的巨噬细胞极化表型，即“M1”和“M2”的背景下定义损伤诱导的炎症反应。在这里，我们扩展了我们以前在脑外伤啮齿动物模型中的工作，以表明炎症反应的分类不能如此容易地用这个命名法来描述。具体地说，我们发现，TBI在促炎和抗炎两个手臂中都引发了广泛的同时表达反应。此外，我们发现，主要负责产生这些炎症介质的细胞，小胶质细胞/巨噬细胞，同时表达“M1”和“M2”表型标记。总体而言，这些数据与最近的报道一致，表明小胶质细胞/巨噬细胞不能充分切换到极化的“仅M1”或“仅M2”表型，但由于周围复杂的信号事件，小胶质细胞/巨噬细胞表现出混合表型。
Following the primary mechanical impact, traumatic brain injury (TBI) induces the simultaneous production of a variety of pro- and anti-inflammatory molecular mediators. Given the variety of cell types and their requisite expression of cognate receptors this creates a highly complex inflammatory milieu. Increasingly in neurotrauma research there has been an effort to define injury-induced inflammatory responses within the context of in vitro defined macrophage polarization phenotypes, known as “M1” and “M2”. Herein, we expand upon our previous work in a rodent model of TBI to show that the categorization of inflammatory response cannot be so easily delineated using this nomenclature. Specifically, we show that TBI elicited a wide spectrum of concurrent expression responses within both pro- and anti-inflammatory arms. Moreover, we show that the cells principally responsible for the production of these inflammatory mediators, microglia/macrophages, simultaneously express both “M1” and “M2” phenotypic markers. Overall, these data align with recent reports suggesting that microglia/macrophages cannot adequately switch to a polarized “M1-only” or “M2-only” phenotype, but display a mixed phenotype due to the complex signaling events surrounding them.