Docosahexaenoic acid impacts macrophage phenotype subsets and phagolysosomal membrane permeability with particle exposure.
Docosahexaenoic acid impacts macrophage phenotype subsets and phagolysosomal membrane permeability with particle exposure.
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Docosahexaenoic Acid会影响巨噬细胞表型亚群和吞噬膜膜的渗透性。
DOI：
10.1080/15287394.2020.1842826
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发表时间：
2021-02-16
期刊：
影响因子：
--
通讯作者：
Holian A
中科院分区：
文献类型：
--
作者：
Fletcher P;Hamilton RF Jr;Rhoderick JF;Pestka JJ;Holian A
吸入颗粒物会导致肺部炎症；然而，目前缺乏治疗方法。二十二碳六烯酸(DHA)是一种omega-3多不饱和脂肪酸，具有抗炎作用。DHA对颗粒诱导的炎症反应的影响尚不清楚，因此，本研究的目的是验证DHA通过改变吞噬体膜通透性(LMP)和改变巨噬细胞表型而下调巨噬细胞炎症反应的假说。分离的Balb/c肺泡巨噬细胞(AM)在体外被极化成M1、M2a、M2b或M2c表型，用DHA处理，并暴露于多壁碳纳米管(MWNCT)或结晶二氧化硅(SiO_2)。结果显示最小的细胞毒性，对二氧化硅颗粒摄取的强烈影响，以及表型之间的LMP差异。二十二碳六烯酸在最大程度上阻止了M2c表型的这些影响。为了确定DHA是否对体内炎症有类似的影响，Balb/c小鼠被置于对照组或1%DHA饲料中3周，滴注相同的颗粒，并在滴注后24小时进行评估。数据显示，与体外研究结果相反，DHA增加了肺部炎症和LMP。这些结果表明，体内的肺反应可能不一定可以从体外的单细胞反应中预测出来。
Inhalation of particles results in pulmonary inflammation; however, treatments are currently lacking. Docosahexaenoic acid (DHA) is an omega-3 polyunsaturated fatty acid shown to exhibit anti-inflammatory capabilities. The impact of DHA on particle-induced inflammation is unclear, therefore, the aim of this study was to examine the hypothesis that DHA downregulates macrophage inflammatory responses by altering phagolysosomal membrane permeability (LMP) and shifting macrophage phenotype. Isolated Balb/c alveolar macrophages (AM) were polarized into M1, M2a, M2b, or M2c phenotypes in vitro, treated with DHA, and exposed to a multi-walled carbon nanotube (MWNCT) or crystalline silica (SiO2). Results showed minimal cytotoxicity, robust effects for silica particle uptake, and LMP differences between phenotypes. Docosahexaenoic acid prevented these effects to the greatest extent in M2c phenotype. To determine if DHA affected inflammation similarly in vivo, Balb/c mice were placed on a control or 1% DHA diet for 3 weeks, instilled with the same particles, and assessed 24hr following instillation. Data demonstrated that in contrast to in vitro findings, DHA increased pulmonary inflammation and LMP. These results suggest that pulmonary responses in vivo may not necessarily be predicted from single cell responses in vitro.
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