Borchsenius Sergei N, Vishnyakov Innokentii E, Chernova Olga A, Chernov Vladislav M, Barlev Nikolai A
Institute of Cytology, Russian Academy of Sciences, 194064 St. Petersburg, Russia.
Kazan Institute of Biochemistry and Biophysics, FRC Kazan Scientific Center, 420111 Kazan, Russia.
Pathogens. 2020 Apr 22;9(4):308. doi: 10.3390/pathogens9040308.
Mycoplasmas are the smallest free-living organisms. Reduced sizes of their genomes put constraints on the ability of these bacteria to live autonomously and make them highly dependent on the nutrients produced by host cells. Importantly, at the organism level, mycoplasmal infections may cause pathological changes to the host, including cancer and severe immunological reactions. At the molecular level, mycoplasmas often activate the NF-κB (nuclear factor kappa-light-chain-enhancer of activated B cells) inflammatory response and concomitantly inhibit the p53-mediated response, which normally triggers the cell cycle and apoptosis. Thus, mycoplasmal infections may be considered as cancer-associated factors. At the same time, mycoplasmas through their membrane lipoproteins (LAMPs) along with lipoprotein derivatives (lipopeptide MALP-2, macrophage-activating lipopeptide-2) are able to modulate anti-inflammatory responses via nuclear translocation and activation of the Nrf2 (nuclear factor-E2-related anti-inflammatory transcription factor 2). Thus, interactions between mycoplasmas and host cells are multifaceted and depend on the cellular context. In this review, we summarize the current information on the role of mycoplasmas in affecting the host's intracellular signaling mediated by the interactions between transcriptional factors p53, Nrf2, and NF-κB. A better understanding of the mechanisms underlying pathologic processes associated with reprogramming eukaryotic cells that arise during the mycoplasma-host cell interaction should facilitate the development of new therapeutic approaches to treat oncogenic and inflammatory processes.
支原体是最小的自由生活生物。其基因组大小的缩减限制了这些细菌自主生存的能力，使它们高度依赖宿主细胞产生的营养物质。重要的是，在生物体水平上，支原体感染可能会导致宿主发生病理变化，包括癌症和严重的免疫反应。在分子水平上，支原体常常激活NF-κB（核因子κB，即活化B细胞的轻链增强子）炎症反应，并同时抑制p53介导的反应，而p53介导的反应通常会触发细胞周期和细胞凋亡。因此，支原体感染可被视为癌症相关因素。同时，支原体通过其膜脂蛋白（LAMPs）以及脂蛋白衍生物（脂肽MALP-2，巨噬细胞激活脂肽-2）能够通过Nrf2（核因子E2相关的抗炎转录因子2）的核转位和激活来调节抗炎反应。因此，支原体与宿主细胞之间的相互作用是多方面的，并且取决于细胞环境。在这篇综述中，我们总结了关于支原体在影响由转录因子p53、Nrf2和NF-κB之间的相互作用介导的宿主细胞内信号传导中所起作用的当前信息。更好地理解支原体与宿主细胞相互作用过程中发生的真核细胞重编程相关病理过程的潜在机制，应该有助于开发治疗致癌和炎症过程的新治疗方法。
