Laboratory of Systems Mucosal Biomodulation, Department of Microbiology and Immunology, Medical Research Institute Pusan National University School of Medicine, Yangsan 626-870, South Korea.
Toxicon. 2012 Jan;59(1):192-204. doi: 10.1016/j.toxicon.2011.11.010. Epub 2011 Nov 19.
Specific ribosome-directed stressors have the capacity to damage 28S ribosomal RNA by interfering with its functioning during gene translation. This can lead to what has been called ribotoxic stress responses that are closely associated with various disease processes including epithelial inflammation in humans and domestic animals. Since the primary toxic actions of most ribotoxic stress agents are generally recognized to be the functional inhibition of global protein synthesis, highly dividing tissues including epithelia are the most susceptible targets of toxic insult. In the present study, responses in the mucosal barrier by acute and chronic exposure to ribosome-inactivating agents were reviewed in various experimental models. Specifically, the focus of this review will be on the regulation of mucosa-associated microbiota, epithelial pro-inflammatory insult, and epithelial integrity. The review aims at characterizing the mechanistic evidence of the ribotoxic stress-induced cellular responses and their implication as critical etiological factors of mucosa-associated diseases, in particular epithelial inflammatory disease.
特定的核糖体靶向应激物能够通过干扰其在基因翻译过程中的功能来破坏 28S 核糖体 RNA。这可能导致所谓的核糖体毒性应激反应，这些反应与各种疾病过程密切相关，包括人类和家畜的上皮炎症。由于大多数核糖体毒性应激剂的主要毒性作用通常被认为是对全球蛋白质合成的功能抑制，因此包括上皮细胞在内的高分裂组织是最容易受到毒性侵害的靶标。在本研究中，综述了各种实验模型中急性和慢性暴露于核糖体失活剂时粘膜屏障的反应。具体来说，本综述的重点将放在粘膜相关微生物群的调节、上皮炎症损伤和上皮完整性上。本综述旨在描述核糖体毒性应激诱导的细胞反应的机制证据及其作为与粘膜相关疾病（特别是上皮炎症性疾病）相关的关键病因因素的意义。
