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白细胞介素1β诱导大鼠肺巨噬细胞炎性蛋白2基因表达

Induction of macrophage inflammatory protein 2 gene expression by interleukin 1 beta in rat lung.

作者信息

Xu W B, Haddad E B, Tsukagoshi H, Adcock I, Barnes P J, Chung K F

机构信息

Department of Thoracic Medicine, National Heart and Lung Institute, London, UK.

出版信息

Thorax. 1995 Nov;50(11):1136-40. doi: 10.1136/thx.50.11.1136.

DOI:10.1136/thx.50.11.1136
PMID:8553267
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC475083/
Abstract

BACKGROUND

Recruitment of inflammatory cells in the lungs may contribute to tissue injury as a result of mediators released from these cells. Interleukin 1 beta (IL-1 beta) is a potent inducer of neutrophil accumulation, a process that may require local protein biosynthesis. Macrophage inflammatory protein 2 (MIP-2) is a approximately 6 kD heparin binding protein and is a member of the C-X-C superfamily that causes significant neutrophil chemotaxis and activation in vitro. A study was performed to determine whether IL-1 beta could induce the expression of MIP-2 in the lungs of Brown-Norway rats.

METHODS

rhIL-1 beta (500 U) or 0.9% NaCl was injected intratracheally and bronchoalveolar lavage (BAL) cells and lung tissues were evaluated for MIP-2 mRNA expression after RNA extraction by Northern blot analysis. MIP-2 probe was prepared from cDNA obtained by reverse transcriptase-polymerase chain reaction (RT-PCR) of BAL cells obtained from a rat treated with lipopolysaccharide.

RESULTS

There was no detectable MIP-2 mRNA in the lungs of control rats but a marked enhancement of the expression at four hours with no expression at 12 hours and a slight expression at 24 hours. IL-1 beta induced a significant influx of neutrophils into BAL fluid with a transient increase in macrophages. In situ hybridisation of lungs using MIP-2 cDNA probe labelled with digoxigenin showed expression of MIP-2 mRNA in airway mononuclear cells and airway epithelium at four hours after IL-1 beta; at 24 hours the signal had nearly gone.

CONCLUSION

IL-1 beta induces the expression of MIP-2 mRNA in rat lung. MIP-2 may be one chemokine that could contribute to IL-1 beta induced neutrophil influx.

摘要

背景

肺部炎症细胞的募集可能因这些细胞释放的介质而导致组织损伤。白细胞介素1β(IL-1β)是中性粒细胞聚集的强效诱导剂,这一过程可能需要局部蛋白质生物合成。巨噬细胞炎性蛋白2(MIP-2)是一种约6kD的肝素结合蛋白,是C-X-C超家族的成员,在体外可引起显著的中性粒细胞趋化和激活。进行了一项研究以确定IL-1β是否能诱导棕色挪威大鼠肺中MIP-2的表达。

方法

经气管内注射重组人IL-1β(500U)或0.9%氯化钠,RNA提取后通过Northern印迹分析评估支气管肺泡灌洗(BAL)细胞和肺组织中MIP-2 mRNA的表达。MIP-2探针由经脂多糖处理的大鼠BAL细胞逆转录聚合酶链反应(RT-PCR)获得的cDNA制备。

结果

对照大鼠肺中未检测到MIP-2 mRNA,但在4小时时表达显著增强,12小时时无表达,24小时时有轻微表达。IL-1β诱导大量中性粒细胞流入BAL液,巨噬细胞短暂增加。使用地高辛标记的MIP-2 cDNA探针进行肺原位杂交显示,IL-1β注射后4小时,气道单核细胞和气道上皮中有MIP-2 mRNA表达;24小时时信号几乎消失。

结论

IL-1β诱导大鼠肺中MIP-2 mRNA的表达。MIP-2可能是一种有助于IL-1β诱导中性粒细胞流入的趋化因子。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/abb8/475083/f6ebece8c8f3/thorax00316-0024-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/abb8/475083/30f42b9b720f/thorax00316-0022-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/abb8/475083/2fb758053c34/thorax00316-0023-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/abb8/475083/f6ebece8c8f3/thorax00316-0024-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/abb8/475083/30f42b9b720f/thorax00316-0022-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/abb8/475083/2fb758053c34/thorax00316-0023-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/abb8/475083/f6ebece8c8f3/thorax00316-0024-a.jpg

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