腺苷和ATP影响lps诱导的巨噬细胞产生细胞因子

Q4 Pharmacology, Toxicology and Pharmaceutics
Kyoko Watanabe, Y. Azuma, S. Shirasu, M. Daito, K. Ohura
{"title":"腺苷和ATP影响lps诱导的巨噬细胞产生细胞因子","authors":"Kyoko Watanabe, Y. Azuma, S. Shirasu, M. Daito, K. Ohura","doi":"10.11263/JSOTP1982.22.105","DOIUrl":null,"url":null,"abstract":"Macrophages are essential for controlling the majority of infections, and are mediators of natural immunity. During infection, lipopolysaccharide (LPS) stimulates macrophages to produce pro-inflammatory cytokines. Adenosine and ATP released into the extracellular space by immunological stimuli have been shown to regulate various immune functions. We evaluate immunological effects of adenosine and ATP on the production of cytokines related to inflammation and Thl/Th2 balance by rat peritoneal macrophages. Adenosine and ATP respectively increased the production of IL-10 without affecting the production of IL-1 ƒÀand IL-12 by macrophages. In addition, adenosine and ATP prevented the production of IL-1 iS and IL-12 by LPSstimulated macrophages. In contrast, adenosine inhibited IL-10 production by LPSstimulated macrophages, whereas ATP potentiated IL-10 production by LPS-stimulated macrophages. These results suggest that conditions related to increased adenosine and/or ATP may play an important role in .a wide range of immune reactions including the Thl and Th2 immune response.","PeriodicalId":19590,"journal":{"name":"Oral Therapeutics and Pharmacology","volume":"22 1","pages":"105-110"},"PeriodicalIF":0.0000,"publicationDate":"2003-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Adenosine and ATP affect LPS-induced cytokine production by macrophages\",\"authors\":\"Kyoko Watanabe, Y. Azuma, S. Shirasu, M. Daito, K. Ohura\",\"doi\":\"10.11263/JSOTP1982.22.105\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"Macrophages are essential for controlling the majority of infections, and are mediators of natural immunity. During infection, lipopolysaccharide (LPS) stimulates macrophages to produce pro-inflammatory cytokines. Adenosine and ATP released into the extracellular space by immunological stimuli have been shown to regulate various immune functions. We evaluate immunological effects of adenosine and ATP on the production of cytokines related to inflammation and Thl/Th2 balance by rat peritoneal macrophages. Adenosine and ATP respectively increased the production of IL-10 without affecting the production of IL-1 ƒÀand IL-12 by macrophages. In addition, adenosine and ATP prevented the production of IL-1 iS and IL-12 by LPSstimulated macrophages. In contrast, adenosine inhibited IL-10 production by LPSstimulated macrophages, whereas ATP potentiated IL-10 production by LPS-stimulated macrophages. These results suggest that conditions related to increased adenosine and/or ATP may play an important role in .a wide range of immune reactions including the Thl and Th2 immune response.\",\"PeriodicalId\":19590,\"journal\":{\"name\":\"Oral Therapeutics and Pharmacology\",\"volume\":\"22 1\",\"pages\":\"105-110\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2003-12-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Oral Therapeutics and Pharmacology\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.11263/JSOTP1982.22.105\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q4\",\"JCRName\":\"Pharmacology, Toxicology and Pharmaceutics\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Oral Therapeutics and Pharmacology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.11263/JSOTP1982.22.105","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"Pharmacology, Toxicology and Pharmaceutics","Score":null,"Total":0}
引用次数: 0

摘要

巨噬细胞是控制大多数感染所必需的,是自然免疫的介质。在感染期间,脂多糖(LPS)刺激巨噬细胞产生促炎细胞因子。免疫刺激释放到细胞外空间的腺苷和ATP已被证明调节各种免疫功能。我们评估了腺苷和ATP对大鼠腹腔巨噬细胞炎症和Thl/Th2平衡相关细胞因子产生的免疫学影响。腺苷和ATP分别增加巨噬细胞IL-10的产生,但不影响IL-1 ƒÀand IL-12的产生。此外,腺苷和ATP可阻止lps刺激的巨噬细胞产生IL-1 iS和IL-12。相反,腺苷抑制lps刺激的巨噬细胞产生IL-10,而ATP增强lps刺激的巨噬细胞产生IL-10。这些结果表明,与腺苷和/或ATP增加相关的条件可能在包括Thl和Th2免疫反应在内的广泛免疫反应中发挥重要作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Adenosine and ATP affect LPS-induced cytokine production by macrophages
Macrophages are essential for controlling the majority of infections, and are mediators of natural immunity. During infection, lipopolysaccharide (LPS) stimulates macrophages to produce pro-inflammatory cytokines. Adenosine and ATP released into the extracellular space by immunological stimuli have been shown to regulate various immune functions. We evaluate immunological effects of adenosine and ATP on the production of cytokines related to inflammation and Thl/Th2 balance by rat peritoneal macrophages. Adenosine and ATP respectively increased the production of IL-10 without affecting the production of IL-1 ƒÀand IL-12 by macrophages. In addition, adenosine and ATP prevented the production of IL-1 iS and IL-12 by LPSstimulated macrophages. In contrast, adenosine inhibited IL-10 production by LPSstimulated macrophages, whereas ATP potentiated IL-10 production by LPS-stimulated macrophages. These results suggest that conditions related to increased adenosine and/or ATP may play an important role in .a wide range of immune reactions including the Thl and Th2 immune response.
求助全文
通过发布文献求助,成功后即可免费获取论文全文。 去求助
来源期刊
Oral Therapeutics and Pharmacology
Oral Therapeutics and Pharmacology Medicine-Pharmacology (medical)
CiteScore
0.10
自引率
0.00%
发文量
0
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信