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由……感染引起的肌肉坏死疾病模型

A Disease Model of Muscle Necrosis Caused by Infection in .

作者信息

Chen Po-Lin, Chen Yi-Wei, Ou Chun-Chun, Lee Tzer-Min, Wu Chi-Jung, Ko Wen-Chien, Chen Chang-Shi

机构信息

Institute of Clinical Medicine, College of Medicine, National Cheng Kung UniversityTainan, Taiwan; Department of Internal Medicine, National Cheng Kung University Hospital, College of Medicine, National Cheng Kung UniversityTainan, Taiwan; Department of Internal Medicine, College of Medicine, National Cheng Kung UniversityTainan, Taiwan.

Institute of Basic Medical Sciences, College of Medicine, National Cheng Kung University Tainan, Taiwan.

出版信息

Front Microbiol. 2017 Jan 4;7:2058. doi: 10.3389/fmicb.2016.02058. eCollection 2016.

Abstract

A variety of bacterial infections cause muscle necrosis in humans. has epidermis and bands of muscle that resemble soft-tissue structures in mammals and humans. Here, we developed a muscle necrosis model caused by infection in . Our data showed that infected and killed rapidly. Characteristic muscle damage in induced by was demonstrated . Relative expression levels of host necrosis-associated genes, , , and increased significantly after infection. The RNAi sensitive NL2099 ) worms with knockdown of necrosis genes of and by RNAi showed prolonged survival after infection. Specifically knockdown of and by RNAi in WM118 worms, which restricted RNAi only to the muscle cells, conferred significant resistance to infection. In contrast, the severity of muscle damage and toxicity produced by the hemolysin-deletion mutant is attenuated. In another example, shiga-like toxin-producing enterohemorrhagic (EHEC) known to elicit toxicity to with concomitant enteropathogenicty, did not cause muscle necrosis as did. Taken together, these results show that infection induces muscle necrosis and rapid death of infected , which are similar to muscle necrosis in humans, and then validate the value of the model with infection in studying pathogenicity.

摘要

多种细菌感染可导致人类肌肉坏死。[具体生物名称]具有表皮和肌肉带,类似于哺乳动物和人类的软组织结构。在此,我们建立了由[具体生物名称]感染引起的[实验对象]肌肉坏死模型。我们的数据表明,[具体生物名称]感染并迅速杀死了[实验对象]。由[具体生物名称]诱导的[实验对象]特征性肌肉损伤得到了证实。感染[具体生物名称]后,宿主坏死相关基因[基因名称1]、[基因名称2]、[基因名称3]和[基因名称4]的相对表达水平显著增加。通过RNAi敲低[具体生物名称]坏死基因的RNAi敏感NL2099([实验对象具体类型])蠕虫在感染[具体生物名称]后存活时间延长。在仅将RNAi限制在肌肉细胞的WM118蠕虫中,通过RNAi特异性敲低[基因名称]和[基因名称],赋予了对[具体生物名称]感染的显著抗性。相比之下,[具体生物名称]溶血素缺失突变体产生的肌肉损伤和毒性的严重程度有所减轻。在另一个例子中,已知产生志贺样毒素的肠出血性[具体生物名称](EHEC)会引发对[实验对象]的毒性并伴有肠道致病性,但它不会像[具体生物名称]那样导致肌肉坏死。综上所述,这些结果表明,[具体生物名称]感染会诱导肌肉坏死和受感染[实验对象]的快速死亡,这与人类的肌肉坏死相似,进而验证了[具体生物名称]感染的[实验对象]模型在研究[具体生物名称]致病性方面的价值。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8afb/5209350/33ceb9191677/fmicb-07-02058-g001.jpg

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