Histidine Kinase QseC in Glaesserella parasuis Enhances the Secretion of Proinflammatory Cytokines by Macrophages via the p38 and NF-κB Signaling Pathways.

DNA and cell biology Pub Date : 2024-09-01 Epub Date: 2024-07-24 DOI:10.1089/dna.2024.0078
Xuefeng Yan, Congwei Gu, Zehui Yu, Mingde Zhao, Lvqin He
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Abstract

The qseC gene is a two-component system that encodes a histidine protein kinase and is highly conserved among different Glaesserella parasuis strains. In this study, we used qRT-PCR and enzyme-linked immunosorbent assay to confirm that Toll-like receptor 4 (TLR4) plays a role in the expression of proinflammatory cytokines interleukin (IL)-1β and IL-6 by stimulating RAW 264.7 macrophages with QseC. Furthermore, we revealed that blocking the p38 and NF-κB pathways that regulate signaling can significantly reduce the production of proinflammatory cytokines induced by QseC. In summary, our data suggest that QseC is a novel proinflammatory mediator that induces TLR4-dependent proinflammatory activity in RAW 264.7 macrophages through the p38 and NF-κB pathways.

寄生褐藻中的组氨酸激酶 QseC 通过 p38 和 NF-κB 信号通路促进巨噬细胞分泌促炎细胞因子。
qseC 基因是一个双组分系统,编码组氨酸蛋白激酶,在不同的寄生褐藻菌株中高度保守。在本研究中,我们利用 qRT-PCR 和酶联免疫吸附试验证实,通过用 QseC 刺激 RAW 264.7 巨噬细胞,Toll 样受体 4(TLR4)在促炎细胞因子白细胞介素(IL)-1β 和 IL-6 的表达中发挥作用。此外,我们还发现,阻断调节信号传导的 p38 和 NF-κB 通路可显著减少 QseC 诱导的促炎细胞因子的产生。总之,我们的数据表明,QseC 是一种新型促炎介质,它能通过 p38 和 NF-κB 通路诱导 RAW 264.7 巨噬细胞产生依赖于 TLR4 的促炎活性。
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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