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沙门菌逃逸宿主天然免疫应答机制的研究进展 被引量:4

Current research progress on host innate immune escaping by Salmonella
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摘要 沙门菌是重要的食源性病原菌,其流行严重威胁着全球公共卫生安全。天然免疫应答对于宿主抵御沙门菌的感染具有重要的作用,但是沙门菌已演化出一系列逃逸宿主天然免疫应答的策略,使其在宿主体内定植,并得以持续性感染。本文对由受体(TLRs、NLRs和RIPs)、细胞因子(IL-22和IL-4)和哺乳动物西罗莫司靶蛋白(mammalian target of rapamycin,mTOR)信号通路介导的沙门菌逃逸天然免疫应答的机制研究进展进行阐述,期望为沙门菌的预防与治疗提供新的研究思路。 Salmonella is an important foodborne pathogen,which seriously threatens the global public health.The host innate immune response plays a significant role for resisting infection.Nowadays,Salmonella has evolved a series of strategies to escape the innate immune response for persistent infections.This review gives a detailed summarization on the new strategies of Salmonella,including receptors(TLRs,NLRs,RIPs),cytokines(IL-22 and IL-4)and mTOR signaling pathway-mediated immune escape.
作者 徐诺 周帮月 史艺 潘兴元 秦涛 徐正中 阴银燕 XU Nuo;ZHOU Bangyue;SHI Yi;PAN Xingyuan;QIN Tao;XU Zhengzhong;YIN Yinyan(Institute of Translational Medicine,Medical College,Yangzhou University,Yangzhou 225009,Jiangsu,China;Jiangsu Key laboratory of integrated traditional Chinese and Western Medicine for prevention and treatment of Senile Diseases,Yangzhou University,Yangzhou 225009,Jiangsu,China;Jiangsu Co-Innovation Center for the Prevention and Control of Important Animal Infectious Disease and Zoonosis,College of Veterinary Medicine,Yangzhou University,Yangzhou 225009,Jiangsu,China;Jiangsu Key Laboratory of Zoonosis,Yangzhou University,Yangzhou 225009,Jiangsu,China)
出处 《微生物与感染》 2020年第5期331-336,共6页 Journal of Microbes and Infections
基金 国家自然科学基金资助项目(31600113) 江苏省人兽共患病学重点实验室资助项目(R1909) 江苏高校优势学科建设工程(PAPD)资助项目。
关键词 沙门菌 免疫逃逸 TOLL样受体 核苷酸结合寡聚化结构域样受体 细胞因子 哺乳动物西罗莫司靶蛋白信号通路 Salmonella Immune evasion Toll like receptor Nucleotide binding oligomerization domain like receptor Cytokines Mammalian target of rapamycin signaling pathway
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  • 1Janeway CA Jr, Medzhitov R. Innate immune recognition. Annu Rev Immuno12002; 20:197-216.
  • 2Chen GY, Nunez G. Sterile inflammation: sensing and react- ing to damage. Nat Rev lmmuno12010; 10:826-837.
  • 3Warburg O, Wind F, Negelein E. The metabolism of tumors in the body. JGen Physiol 1927; 8:519-530.
  • 4Sbarra AJ, Karnovsky ML. The biochemical basis of phago- cytosis. I. Metabolic changes during the ingestion of parti- cles by polymorphonuclear leukocytes. J Biol Chem 1959; 234:1355-1362.
  • 5Guthrie LA, McPhail LC, Henson PM, Johnston Jr RB. Prim- ing of neutrophils for enhanced release of oxygen metabolites by bacterial lipopolysaccharide. Evidence for increased ac- tivity of the superoxide-producing enzyme. J Exp Med 1984; 160:1656-1671.
  • 6Borregaard N, Herlin T. Energy metabolism of human neutro- phils during phagocytosis. J Clin Invest 1982; 70:550-557.
  • 7Hard GC. Some biochemical aspects of the immune macro- phage. BrJExp Pathol 1970; 51:97-105.
  • 8Newsholme P, Gordon S, Newsholme EA. Rates of utiliza- tion and fates of glucose, glutamine, pyruvate, fatty acids and ketone bodies by mouse macrophages. Biochem J 1987; 242:631-636.
  • 9Newsholme P, Curi R, Gordon S, Newsholme EA. Metabo- lism of glucose, glutamine, long-chain fatty acids and ketone bodies by murine macrophages. Biochem J 1986; 239:121- 125.
  • 10Krawczyk CM, Holowka T, Sun J, et al. Toll-like receptor-in- duced changes in glycolytic metabolism regulate dendritic cell activation. Blood 2010; 115:4742-4749.

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