IF 3.3 3区 生物学 Q3 CELL BIOLOGY
Xiao-Min Fang, Xing-Jian Liu, Rui-Gang Zhang
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引用次数: 0

摘要

一氧化碳(CO)是一种新型抗炎分子,但一氧化碳对 SARS-CoV-2 穗状 RBD(S-RBD)诱导的人类支气管上皮细胞因子释放的影响仍不清楚。CO释放分子3(CORM-3)可释放CO。在 16HBE14o- 人支气管上皮细胞系中,通过酶联免疫吸附试验(ELISA)测定了 S-RBD、ATPγS 和 CO 对细胞因子分泌的影响。通过 Western 印迹分析评估了 CO 对 S-RBD 诱导的 ERK 磷酸化的抑制作用。通过短路电流(ISC)量化了 CO 对细胞外 nuleotide 诱导的离子转运的调节作用。S-RBD 可诱导 CCL5 和 IL-6 的释放,CO 可抑制这种效应。然而,CO 未能抑制 S-RBD 诱导的 ATP 释放,但却降低了 ATP 诱导的 CCL5 和 IL-6 分泌以及离子转运。此外,CO 还能明显抑制 S-RBD 诱导的 ERK 磷酸化。这些研究结果表明,CO 在 S-RBD 和细胞外核苷酸诱导的人支气管上皮细胞炎症过程中具有抗炎作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Carbon monoxide inhibits human bronchial epithelial CCL5 and IL-6 secretion induced by SARS-CoV-2 spike RBD protein
Carbon monoxide (CO) is a novel anti-inflammatory molecule, but the effects of CO on SARS-CoV-2 spike RBD (S-RBD)-induced human bronchial epithelial cytokines release remains unclear. CO was delivered using CO-releasing molecule 3 (CORM-3). The effects of S-RBD, ATPγS and CO on cytokines secretion were determined by enzyme-linked immunosorbent assay (ELISA) in 16HBE14o-human bronchial epithelial cell line. The inhibitory effect of CO on S-RBD-induced ERK phosphorylation was assessed by Western blot analysis. The regulatory effect of CO on extracellular nucleotide-induced ion transport was quantified by short-circuit current (ISC). S-RBD evoked CCL5 and IL-6 release and this effect could be suppressed by CO. However, CO failed to inhibit ATP release induced by S-RBD while decreased ATP-induced CCL5 and IL-6 secretion as well as ion transport. Furthermore, CO significantly inhibited ERK phosphorylation induced by S-RBD. These findings suggest an anti-inflammatory role of CO during inflammation induced by S-RBD and extracellular nucleotide in human bronchiol epithelial cells.
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来源期刊
Experimental cell research
Experimental cell research 医学-细胞生物学
CiteScore
7.20
自引率
0.00%
发文量
295
审稿时长
30 days
期刊介绍: Our scope includes but is not limited to areas such as: Chromosome biology; Chromatin and epigenetics; DNA repair; Gene regulation; Nuclear import-export; RNA processing; Non-coding RNAs; Organelle biology; The cytoskeleton; Intracellular trafficking; Cell-cell and cell-matrix interactions; Cell motility and migration; Cell proliferation; Cellular differentiation; Signal transduction; Programmed cell death.
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