权益分类	功能权益	普通用户	{{item.name}}会员
{{category.name}}	{{benefitItem.name}}

Comparative studies of the effect of adenosine and ATP affect LPS induced inflammation

腺苷和ATP影响LPS诱导炎症作用的比较研究

基本信息

批准号：
15591987
负责人：
OHURA Kiyoshi
金额：
$ 2.24万
依托单位：
Osaka Dental University
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
2003
资助国家：
日本
起止时间：
2003 至 2004
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-15591987/
关键词：
A2a adenosine receptor Toll like receptor adenosine ATP LPS inflammation cytokine differentiation

项目摘要

Macriphages are essential for controlling the majority of infections, and are mediators of natural immunity. During an infection, lipopolysaccharide (LPS) stimulates macrophages to produce proinflanimatory cytokines. Recently, it has been shown that A 2aadenosinereceptor (A2 aiR) is a critical part of the physiological negative feedback mechanism for the limitation and termination of tissue-specific and systemic inflammatory rsponseis It was useful and meaningful to gain information about interaction between LPS, which generates the inflammation, and adenosine receptors, which terminate the the inflamation. However, very little, if anything, is known about the effect of bacterial LPS on the expretion of A2aR during an infection of bacteria. The aim of this study is to evaluate the effect of adenosine,ATPand LPS on the espression of A2aR and LPS on the expression of A2aR and toll-like receptor 4(TLR4), which is a receptor for LPS, in the mouse macropharge cell line RAW 264. Adenosine and ATP failed to affect prolifaration in RAW 264 cells, whereas LPS increased proliferation. Adenosine significantly protentiated potentiated the expression of TLR4, hut not of A2aR ATP and LPS, markedly potentiated of the expression of A2aR and TLR4 in the presence of LPS, respenctively. Moreover adenosine and ATP did not affect the expression of A2aR and TLR 4 in the presences of LPS, respenctively. This study revealed that adenosine, ATP and LPS affect the exprettion of A2aR and TLR4 in macrophages.

巨噬细胞对于控制大多数感染是必不可少的，并且是天然免疫的介质。在感染过程中，脂多糖（LPS）刺激巨噬细胞产生促炎症细胞因子。近年来研究表明，腺苷受体A2（A2 aadenosinereceptor，A2 aIR）是限制和终止组织特异性和全身性炎症反应的生理负反馈机制的重要组成部分。然而，在细菌感染过程中，细菌LPS对A2 aR表达的影响知之甚少。本研究旨在探讨腺苷、ATP和LPS对小鼠巨噬细胞系RAW 264中A2 aR表达的影响以及LPS对A2 aR和LPS受体TLR 4表达的影响。腺苷和ATP不能影响RAW 264细胞的增殖，而LPS促进增殖。腺苷可显著增强TLR 4的表达，但对A2 aR、ATP和LPS的表达无明显影响;腺苷可显著增强A2 aR和TLR 4在LPS存在下的表达。腺苷和ATP对LPS刺激下A2 aR和TLR 4的表达无明显影响。腺苷、ATP和LPS均可影响巨噬细胞A2 aR和TLR 4的表达。