细菌膜囊泡通过抑制线粒体复合物III激活单磷酸腺苷激活的蛋白激酶信号通路。

Bacterial membrane vesicles of activate adenosine monophosphate-activated protein kinase signaling through inhibition of mitochondrial complex III.

作者信息

Müller Julia, Kretschmer Marcel, Opitsch Elise, Holland Svea, Borrero-de Acuña José Manuel, Jahn Dieter, Neumann-Schaal Meina, Wegner Andre

机构信息

Braunschweig Integrated Centre of Systems Biology (BRICS), Technische Universität Braunschweig, Rebenring 56, 38106 Braunschweig, Germany.

Department of Bioinformatics and Biochemistry, Technische Universität Braunschweig, Rebenring 56, 38106 Braunschweig, Germany.

出版信息

PNAS Nexus. 2025 Aug 19;4(8):pgaf248. doi: 10.1093/pnasnexus/pgaf248. eCollection 2025 Aug.

Abstract

Bacterial membrane vesicles (BMVs) are secreted by many pathogenic bacteria and known to stimulate various host responses upon infection, thereby contributing to the pathogenicity of bacterial pathogens like . While the effects of BMVs on host immune responses are well studied, little is known about their impact on cell metabolism and mitochondrial respiration. Here, we show that BMVs (i) reprogram cell metabolism of human lung cells, (ii) negatively affect mitochondrial respiration by (iii) specifically inhibiting complex III of the electron transport chain, leading to (iv) the activation of adenosine monophosphate-activated protein kinase (AMPK) signaling, which in turn results in (v) AMPK-dependent inhibition of global protein synthesis.

摘要

细菌膜泡(BMVs)由许多病原菌分泌,已知在感染时会刺激宿主产生各种反应,从而导致诸如[病原菌名称未给出]等细菌病原体的致病性。虽然BMVs对宿主免疫反应的影响已得到充分研究,但它们对细胞代谢和线粒体呼吸的影响却知之甚少。在这里,我们表明BMVs(i)重新编程人肺细胞的细胞代谢,(ii)通过(iii)特异性抑制电子传递链的复合体III对线粒体呼吸产生负面影响,导致(iv)腺苷单磷酸激活蛋白激酶(AMPK)信号通路的激活,这进而导致(v)AMPK依赖的整体蛋白质合成抑制。

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