Carbon monoxide inhibits human bronchial epithelial CCL5 and IL-6 secretion induced by SARS-CoV-2 spike RBD protein

IF 3.3 3区生物学 Q3 CELL BIOLOGY

Experimental cell research Pub Date : 2025-03-07 DOI:10.1016/j.yexcr.2025.114499

Xiao-Min Fang, Xing-Jian Liu, Rui-Gang Zhang

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引用次数: 0

Abstract

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 (I_SC). 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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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。

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来源期刊

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.