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金黄色葡萄球菌感染中IL-17的分子机制研究进展    

Research progress in the molecular mechanism of interleukin-17 in Staphy - lococcus aureus infection

文献类型:期刊文献

中文题名:金黄色葡萄球菌感染中IL-17的分子机制研究进展

英文题名:Research progress in the molecular mechanism of interleukin-17 in Staphy - lococcus aureus infection

作者:崔岩[1];王天明[1];付琦[1];吴志航[1];李日成[1];陈全鑫[1];刘美[1];王波[2];潘海邦[1]

第一作者:崔岩

机构:[1]甘肃中医药大学第一临床医学院,甘肃兰州730000;[2]甘肃中医药大学护理学院,甘肃兰州730000

第一机构:甘肃中医药大学临床医学院

年份:2023

卷号:22

期号:6

起止页码:731

中文期刊名:中国感染控制杂志

外文期刊名:Chinese Journal of Infection Control

收录:CSTPCD;;北大核心:【北大核心2020】;CSCD:【CSCD2023_2024】;

基金:国家自然科学基金项目(81860850);甘肃省教育厅优秀研究生“创新之星”项目(2021CXZX-734、2021CXZX-736);甘肃省教育厅重大项目《“校院共建”人才培养模式改革及实践探索》资助(研究生“创新基金”项目LCCX2021002)。

语种:中文

中文关键词:金黄色葡萄球菌;白细胞介素-17;分子机制;感染;免疫;IL-17

外文关键词:Staphylococcus aureus;interleukin-17;molecular mechanism;infection;immunity;IL-17

摘要:金黄色葡萄球菌(SA)是当前全球常见的感染性致病菌,抗菌药物的滥用导致SA感染的预防和治疗更加困难。寻求新型有效的抗菌药物替代品或者疫苗至关重要,这也是目前乃至未来研究的热点。大量研究报道白细胞介素-17(IL-17)对于SA的清除和预防至关重要,IL-17家族种类繁多、机制复杂,人体IL-17与SA携带之间的联系虽尚未被广泛研究,但大多数的动物试验结果也带来了克服SA感染的希望。IL-17信号通路的优势也驱使着越来越多的科研人员开始关注其在免疫方面的作用,有望成为抗SA疫苗制剂的关键靶点。本文对IL-17及其信号通路、与SA感染的分子机制的研究进展进行综述。
Staphylococcus aureus(SA)is a common infectious pathogen globally.The misuse of antimicrobial agents has made the prevention and treatment of SA infection more difficult.Seeking new and effective alternatives to antimicrobial agents is important and is a hot topic in current and future research.Numerous studies have reported that interleukin-17(IL-17)is essential for the clearance and prevention of SA.The IL-17 family is diverse and the mechanism is complex.Although the connection between human IL-17 and SA-carriage has not been widely studied,most animal experimental results have brought hope for overcoming SA infection.The advantages of the IL-17 signaling pathway have also prompted more and more researchers to focus on its role in immunity,with the potential to become a key target of anti-SA vaccine preparation.This paper reviews research progress of IL-17 and its signaling pathway,as well as the molecular mechanism of SA infection.

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