2023年2月，西部特色生物資源保護(hù)與利用教育部重點(diǎn)實驗室;寧夏大學(xué)生命科學(xué)學(xué)院；寧夏銀川市賀蘭山路(Key Lab of Ministry of Education for Protection and Utilization of Special Biological Resources in Western China, Yinchuan 750021, Ningxia, China；School of Life Sciences, Ningxia University, 539 W.  Helanshan Road, Yinchuan 750021, Ningxia, China) Zhanyou Liu老師研究團(tuán)隊在《Scientifc Reports》上發(fā)表論文：

“DUSP1 mediates BCG induced apoptosis and inflammatory response in THP-1 cells via MAPKs/NF-κB signaling pathway"

“DUSP1通過MAPKs/NF-κB信號通路介導(dǎo)BCG誘導(dǎo)的THP-1細(xì)胞凋亡和炎癥反應(yīng)"

Abstract：

Tuberculosis (TB) is a zoonotic infectious disease caused by Mycobacterium tuberculosis (Mtb). Apoptosis and necrosis caused by the interaction between the host and the pathogen, as well as the host's inflammatory response, play an important role in the pathogenesis of TB. Dual-specificity phosphatase 1 (DUSP1) plays a vital role in regulating the host immune responses. However, the role of DUSP1 in the regulation of THP-1 macrophage apoptosis induced by attenuated Mycobacterium bovis Bacillus Calmette-Guérin (BCG) infection remains unclear. In the present study, we report that infection with BCG significantly induces macrophage apoptosis and induces the production of DUSP1, TNF-α and IL-1β. DUSP1 knockdown significantly inhibited BCG-induced macrophage apoptosis and activation of MAPKs/NF-κB signaling pathway. In addition, DUSP1 knockdown suppressed BCG-induced inflammation in vivo. Taken together, this study demonstrates that DUSP1, as a regulator of MAPKs/NF-κB signaling pathway, plays a novel role in BCG-induced macrophage apoptosis and inflammatory response.

摘要：

結(jié)核病(TB)是由結(jié)核分枝桿菌(Mtb)引起的人畜共患傳染病。宿主與病原體相互作用引起的細(xì)胞凋亡和壞死以及宿主的炎癥反應(yīng)在TB的發(fā)病機(jī)制中起著重要作用。雙特異性磷酸酶1 (DUSP1)在調(diào)節(jié)宿主免疫應(yīng)答中起著至關(guān)重要的作用。然而，DUSP1在弱毒牛分枝桿菌卡介苗感染誘導(dǎo)的THP-1巨噬細(xì)胞凋亡中的作用尚不清楚。在本研究中，我們報道了卡介苗感染可顯著誘導(dǎo)巨噬細(xì)胞凋亡并誘導(dǎo)DUSP1、TNF-α和IL-1β的產(chǎn)生。DUSP1基因敲低可顯著抑制bcg誘導(dǎo)的巨噬細(xì)胞凋亡和MAPKs/NF-κB信號通路的激活。此外，DUSP1敲低可抑制bcg誘導(dǎo)的體內(nèi)炎癥。綜上所述，本研究表明DUSP1作為MAPKs/NF-κB信號通路的調(diào)節(jié)因子，在bcg誘導(dǎo)的巨噬細(xì)胞凋亡和炎癥反應(yīng)中發(fā)揮了新的作用。

該論文中，人髓系白血病單核細(xì)胞THP-1細(xì)胞的體外培養(yǎng)是使用Ausbian特級胎牛血清完成的。