Lipopolysaccharide activates the kallikrein–kinin system in mouse choroid plexus cell line ECPC4

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• 作者：Masaoki Takano ; Chieko Satoh ; Naomi Kunimatsu ; Mieko Otani ; Michiko Hamada-Kanazawa ; Masaharu Miyake ; KyongSong Ming ; Katsutoshi Yayama ; Hiroshi Okamoto
• 关键词：Choroid plexus ; Kallikrein– ; kinin ; IL-1β ; TNF- ; //www.sciencedirect.com/scidirimg/entities/204e.gif"" alt=""greek small letter alpha"" title=""greek small letter alpha"" border=""0""> ; Lipopolysaccharide ; ECPC4
• 刊名：Neuroscience Letters
• 出版年：2008
• 出版时间：4 April 2008
• 年：2008
• 卷：434
• 期：3
• 页码：310-314
• 全文大小：311 K

文摘

Regulation of the kallikrein–kinin system in cerebral inflammation is still unclear. Here, we used reverse-transcription polymerase chain reaction (RT-PCR) techniques to show that lipopolysaccharide (LPS) activates the kallikrein–kinin system by enhancing liberation of bradykinin (BK), and alters mRNA levels of kallikrein–kinin system components, including high molecular weight (H-) and low molecular weight (L-) kininogens, in ECPC4 cells, a cell line of mouse choroid plexus epithelium. LPS treatment increased liberation of immunoreactive bradykinin in the supernatant of ECPC4 cells, and addition of LPS (500 ng/ml) to cultures resulted in elevation of H- and L-kininogen mRNA levels in ECPC4 cells within 24–48 h. Furthermore, LPS treatment elevated bradykinin type 2 and type 1 receptor mRNA levels within 4 h, but did not change tissue kallikrein or plasma kallikrein mRNA levels. On the other hand, expression of pro-inflammatory mediators interleukin-1β (IL-1β), tumor necrosis factor- (TNF-), and cyclooxygenase-2 mRNA increased within 4–8 h after addition of LPS to ECPC4 cells. The addition of IL-1β and TNF- to investigate the major mediator for kininogen expression in ECPC4 cells remarkably induced expression of H- and L-kininogen mRNAs in ECPC4 cells. These results suggest that LPS activates the kallikrein–kinin system in the choroid plexus via autocrine induction of IL-1β and TNF-.