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。

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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引用次数: 0

摘要

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

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.

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Radiation-Induced Intestinal Injury: Molecular Mechanisms and Therapeutic Status. The Role of Neddylation in Malaria Parasites. Polo-Like Kinase 1 and DNA Damage Response. Innovating Cancer Treatment Through Cell Cycle, Telomerase, Angiogenesis, and Metastasis. Histidine Kinase QseC in Glaesserella parasuis Enhances the Secretion of Proinflammatory Cytokines by Macrophages via the p38 and NF-κB Signaling Pathways.
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