Institute of Biophysics, CNR Unit at Trento, Via Sommarive 18, Povo Trento 38123, Italy.
Yale Cancer Center, Yale University School of Medicine, New Haven, CT 06520, USA.
Toxins (Basel). 2017 Nov 3;9(11):357. doi: 10.3390/toxins9110357.
Pathogenic bacteria produce powerful virulent factors, such as pore-forming toxins, that promote their survival and cause serious damage to the host. Host cells reply to membrane stresses and ionic imbalance by modifying gene expression at the epigenetic, transcriptional and translational level, to recover from the toxin attack. The fact that the majority of the human transcriptome encodes for non-coding RNAs (ncRNAs) raises the question: do host cells deploy non-coding transcripts to rapidly control the most energy-consuming process in cells-i.e., host translation-to counteract the infection? Here, we discuss the intriguing possibility that membrane-damaging toxins induce, in the host, the expression of toxin-specific long non-coding RNAs (lncRNAs), which act as sponges for other molecules, encoding small peptides or binding target mRNAs to depress their translation efficiency. Unravelling the function of host-produced lncRNAs upon bacterial infection or membrane damage requires an improved understanding of host lncRNA expression patterns, their association with polysomes and their function during this stress. This field of investigation holds a unique opportunity to reveal unpredicted scenarios and novel approaches to counteract antibiotic-resistant infections.
致病细菌会产生强大的毒力因子，如孔形成毒素，这些因子有助于它们的存活并对宿主造成严重损害。宿主细胞通过在表观遗传、转录和翻译水平上改变基因表达来应对膜应激和离子失衡，从而从毒素攻击中恢复。事实上，人类转录组的大部分编码非编码 RNA（ncRNA），这就提出了一个问题：宿主细胞是否会利用非编码转录本来快速控制细胞中最耗能的过程——即宿主翻译——以抵抗感染？在这里，我们讨论了一个有趣的可能性，即膜损伤毒素会诱导宿主表达特定的长非编码 RNA（lncRNA），这些 lncRNA 可以作为其他分子的海绵，编码小肽或结合靶 mRNA 以降低其翻译效率。要了解细菌感染或膜损伤后宿主产生的 lncRNA 的功能，需要更好地了解宿主 lncRNA 的表达模式、它们与多核糖体的关联以及它们在这种应激下的功能。这一研究领域为揭示意想不到的情况和对抗抗生素耐药性感染的新方法提供了独特的机会。
