Macrophage ICAM-1 functions as a regulator of phagocytosis in LPS induced endotoxemia.
Macrophage ICAM-1 functions as a regulator of phagocytosis in LPS induced endotoxemia.
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巨噬细胞 ICAM-1 在 LPS 诱导的内毒素血症中充当吞噬作用的调节因子
DOI：
10.1007/s00011-021-01437-2
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发表时间：
2021-03
期刊：
影响因子：
--
通讯作者：
Tang J
中科院分区：
文献类型：
--
作者：
Zhong H;Lin H;Pang Q;Zhuang J;Liu X;Li X;Liu J;Tang J
细胞内粘附分子-1（ICAM-1）是免疫球蛋白超家族的一种跨膜糖蛋白，在免疫应答过程中介导细胞间相互作用和细胞外信号传导中起着关键作用。ICAM-1在包括内皮细胞、上皮细胞、白细胞、成纤维细胞和嗜中性粒细胞的几种细胞类型的细胞表面上表达。尽管已经在巨噬细胞上检测到ICAM-1，但对巨噬细胞ICAM-1的功能和机制知之甚少。为了探讨脂多糖（LPS）在ICAM-1调节中的作用，检测了ICAM-1的蛋白和细胞表面表达。用流式细胞仪和共聚焦显微镜观察巨噬细胞的吞噬功能。采用小干扰RNA和ICAM-1中和抗体检测ICAM-1对巨噬细胞吞噬功能的影响。采用TLR 4基因敲除小鼠及胞浆和线粒体ROS清除剂对ICAM-1表达进行调控。使用流式细胞术测定ROS。在本研究中，我们报道了LPS可以刺激巨噬细胞增加ICAM-1的蛋白和细胞表面表达。巨噬细胞ICAM-1表达与巨噬细胞吞噬功能增强相关。我们发现，用ICAM-1中和抗体或ICAM-1沉默来减弱ICAM-1的功能或表达，可以降低LPS诱导的巨噬细胞吞噬功能。此外，我们发现，敲除TLR 4导致细胞质和线粒体ROS的产生受到抑制，这反过来又在蛋白质和细胞表面水平上减弱了ICAM-1的表达。这项研究表明，ICAM-1介导的巨噬细胞吞噬作用的机制是依赖于TLR 4介导的ROS的生产，并提供了显着的光巨噬细胞ICAM-1在内毒素血症。
Intracellular adhesion molecule-1 (ICAM-1), a transmembrane glycoprotein belonging to the immunoglobulin superfamily, plays a critical role in mediating cell–cell interaction and outside-in cell signaling during the immune response. ICAM-1 is expressed on the cell surface of several cell types including endothelial cells, epithelial cells, leucocytes, fibroblasts, and neutrophils. Despite ICAM-1 has been detected on macrophage, little is known about the function and mechanism of macrophage ICAM-1. To investigate the role of lipopolysaccharide (LPS) in ICAM-1 regulation, both the protein and cell surface expression of ICAM-1 were measured. The phagocytosis of macrophage was evaluated by flow cytometry and Confocal microscopy. Small interfering RNA and neutralizing antibody of ICAM-1 were used to assess the effect of ICAM-1 on macrophage phagocytosis. TLR4 gene knockout mouse and cytoplasmic and mitochondrial ROS scavenger were used for the regulation of ICAM-1 expression. ROS was determined using flow cytometry. In this study, we reported that macrophage can be stimulated to increase both the protein and cell surface expression of ICAM-1 by LPS. Macrophage ICAM-1 expression was correlated with enhanced macrophage phagocytosis. We found that using ICAM-1 neutralizing antibody or ICAM-1 silencing to attenuate the function or expression of ICAM-1 could decrease LPS-induced macrophage phagocytosis. Furthermore, we found that knocking out of TLR4 led to inhibited cytoplasmic and mitochondrial ROS production, which in turn, attenuated ICAM-1 expression at both the protein and cell surface levels. This study demonstrates that the mechanism of ICAM-1-mediated macrophage phagocytosis is depending on TLR4-mediated ROS production and provides significant light on macrophage ICAM-1 in endotoxemia.
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影响因子：
5.1
作者：
Hubbard, AK;Giardina, C
通讯作者：
Giardina, C
影响因子：
158.5
作者：
Kaukonen, Kirsi-Maija;Bailey, Michael;Bellomo, Rinaldo
通讯作者：
Bellomo, Rinaldo
影响因子：
3.7
作者：
KAPLAN, G
通讯作者：
KAPLAN, G
DOI：
10.1038/nri3073
发表时间：
2011-10-14
期刊：
Nature reviews. Immunology
影响因子：
--
作者：
通讯作者：
--
影响因子：
5.5
作者：
Ode Y;Aziz M;Wang P
通讯作者：
Wang P