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P2Y(6)核苷酸受体介导单核细胞在响应UDP或脂多糖时产生白细胞介素-8。

P2Y(6) nucleotide receptor mediates monocyte interleukin-8 production in response to UDP or lipopolysaccharide.

作者信息

Warny M, Aboudola S, Robson S C, Sévigny J, Communi D, Soltoff S P, Kelly C P

机构信息

Gastroenterology Divison, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02215, USA.

出版信息

J Biol Chem. 2001 Jul 13;276(28):26051-6. doi: 10.1074/jbc.M102568200. Epub 2001 May 10.

Abstract

Extracellular nucleotides are autocrine and paracrine cellular mediators that signal through P2 nucleotide receptors. Monocytic cells express several P2Y receptors but the role of these G protein-coupled receptors in monocytes is not known. Here, we present evidence that P2Y(6) regulates chemokine production and release in monocytes. We find that UDP, a selective P2Y(6) agonist, stimulates interleukin (IL)-8 release in human THP-1 monocytic cells whereas other nucleotides are relatively inactive. P2 receptor antagonists or P2Y(6) antisense oligonucleotides inhibit IL-8 release induced by UDP. Furthermore, UDP specifically activated IL-8 production in astrocytoma 1321N1 cells transfected with human P2Y(6). Since lipopolysaccharide has been suggested to activate P2 receptors via nucleotide release, we tested whether IL-8 production stimulated by lipopolysaccharide might result from P2Y(6) activation. P2 antagonists or apyrase, an enzyme which hydrolyzes nucleotides including UDP, inhibit IL-8 production induced by lipopolysaccharide but not by other stimuli. Furthermore, IL-8 gene expression activated by lipopolysaccharide is enhanced by P2Y(6) overexpression and inhibited by P2Y(6) antisense oligonucleotides. Thus, UDP activates IL-8 production via P2Y(6) in monocytic cells. Furthermore, lipopolysaccharide mediates IL-8 production at least in part by autocrine P2Y(6) activation. These findings indicate a novel role for P2Y(6) in innate immune defenses.

摘要

细胞外核苷酸是通过P2核苷酸受体发出信号的自分泌和旁分泌细胞介质。单核细胞表达多种P2Y受体,但这些G蛋白偶联受体在单核细胞中的作用尚不清楚。在此,我们提供证据表明P2Y(6)调节单核细胞中趋化因子的产生和释放。我们发现,UDP作为一种选择性P2Y(6)激动剂,可刺激人THP-1单核细胞中白细胞介素(IL)-8的释放,而其他核苷酸则相对无活性。P2受体拮抗剂或P2Y(6)反义寡核苷酸可抑制UDP诱导的IL-8释放。此外,UDP可特异性激活转染了人P2Y(6)的星形细胞瘤1321N1细胞中IL-8的产生。由于有人提出脂多糖可通过核苷酸释放激活P2受体,我们测试了脂多糖刺激的IL-8产生是否可能由P2Y(6)激活所致。P2拮抗剂或Apyrase(一种水解包括UDP在内的核苷酸的酶)可抑制脂多糖诱导的IL-8产生,但不抑制其他刺激诱导的IL-8产生。此外,脂多糖激活的IL-8基因表达可被P2Y(6)过表达增强,并被P2Y(6)反义寡核苷酸抑制。因此,UDP通过P2Y(6)在单核细胞中激活IL-8的产生。此外,脂多糖至少部分通过自分泌P2Y(6)激活介导IL-8的产生。这些发现表明P2Y(6)在先天免疫防御中具有新的作用。

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