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体内高锰酸钾(KMnO₄)诱导的慢性炎症状态下单核细胞趋化蛋白-1及其mRNA转录物的增加。

Augmentation of monocyte chemotactic protein-1 and mRNA transcript in chronic inflammatory states induced by potassium permanganate (KMnO4) in vivo.

作者信息

Conti P, Reale M, Feliciani C, Frydas S, Trakatellis M, Placido F C, Cataldo I, Di Gioacchino M, Barbacane R C

机构信息

Immunology Division, University of Chieti Medical School, Italy.

出版信息

Immunology. 1997 Oct;92(2):300-6. doi: 10.1046/j.1365-2567.1997.00329.x.

DOI:10.1046/j.1365-2567.1997.00329.x
PMID:9415040
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1364072/
Abstract

Monocyte chemotactic protein-1 (MCP-1) is a proinflammatory cytokine that attracts and activates specific types of leucocytes. The purpose of this work was to analyse the generation of MCP-1 and mRNA transcript in a model of chronic inflammation using a granulomatous tissue induced by potassium permanganate (KMnO4; water soluble crystals). The data presented here shows that MCP-1 is generated in granuloma tissue and its level was strongly increased by i.p. injections of lipopolysaccharide (LPS) and inhibited in rats treated with injections of dexamethasone, 18 hr before the animals were killed. In histological studies LPS and dexamethasone increased and decreased, respectively, the recruitment of mononuclear cells in the granuloma tissue compared with the control granulomas from phosphate-buffered saline (PBS)-treated animals. Reverse transcriptase-polymerase chain reaction (RT-PCR) was used for mRNA extraction and cDNA synthesis. mRNA MCP-1 was significantly produced in the granuloma tissue of untreated animals, an effect increased by LPS and inhibited by dexamethasone, compared with the controls. Moreover, MCP-1 protein was found in the supernatant from homogenized granuloma tissues and the levels of MCP-1 were higher in the LPS-treated animals, while they were lower in the dexamethasone group, compared with the granulomas from the PBS-treated groups (control). The generation of MCP-1 was also found in minced granuloma tissue incubated for 18 hr (overnight) from treated (LPS or dexamethasone) and untreated (PBS) rats. When LPS was added in vitro for 18 hr to the controls and treated animals the production of MCP-1 was further increased except in the dexamethasone group (P > 0.05). Analysing blood serum from LPS, dexamethasone or PBS-treated rats, we found that MCP-1 was also present. The level was higher in the LPS group and lower in the dexamethasone group, compared with the control (PBS). In these studies we show for the first time that MCP-1 transcript and translation is generated in chronic experimental inflammatory tissue, an effect inhibited by dexamethasone.

摘要

单核细胞趋化蛋白-1(MCP-1)是一种促炎细胞因子,可吸引并激活特定类型的白细胞。本研究的目的是利用高锰酸钾(KMnO4;水溶性晶体)诱导的肉芽肿组织,分析慢性炎症模型中MCP-1及其mRNA转录本的生成情况。本文提供的数据表明,MCP-1在肉芽肿组织中生成,腹腔注射脂多糖(LPS)可使其水平显著升高,而在处死动物前18小时注射地塞米松的大鼠中,MCP-1水平受到抑制。组织学研究表明,与磷酸盐缓冲盐水(PBS)处理动物的对照肉芽肿相比,LPS和地塞米松分别增加和减少了肉芽肿组织中单核细胞的募集。逆转录聚合酶链反应(RT-PCR)用于mRNA提取和cDNA合成。与对照组相比,未处理动物的肉芽肿组织中显著产生了mRNA MCP-1,LPS可增强这一效应,而地塞米松则抑制该效应。此外,在匀浆肉芽肿组织的上清液中发现了MCP-1蛋白,与PBS处理组(对照)的肉芽肿相比,LPS处理动物的MCP-1水平较高,而地塞米松组的MCP-1水平较低。在来自处理过(LPS或地塞米松)和未处理(PBS)大鼠的肉芽肿组织切碎物中孵育18小时(过夜)后,也发现了MCP-1的生成。当在体外向对照组和处理动物中添加LPS 18小时时,除地塞米松组外(P>0.05),MCP-1的产生进一步增加。分析LPS、地塞米松或PBS处理大鼠的血清,我们发现其中也存在MCP-1。与对照组(PBS)相比,LPS组的水平较高,地塞米松组的水平较低。在这些研究中,我们首次表明MCP-1转录本和翻译在慢性实验性炎症组织中生成,这一效应受到地塞米松的抑制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa8a/1364072/a17116f5ff1c/immunology00050-0146-c.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa8a/1364072/36bc01ad2c69/immunology00050-0145-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa8a/1364072/15e8b72e5b43/immunology00050-0146-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa8a/1364072/19b8b942bdb4/immunology00050-0146-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa8a/1364072/a17116f5ff1c/immunology00050-0146-c.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa8a/1364072/36bc01ad2c69/immunology00050-0145-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa8a/1364072/15e8b72e5b43/immunology00050-0146-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa8a/1364072/19b8b942bdb4/immunology00050-0146-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa8a/1364072/a17116f5ff1c/immunology00050-0146-c.jpg

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