論文

査読有り
2004年4月

Histamine production via mast cell-independent induction of histidine decarboxylase in response to lipopolysaccharide and interleukin-1

INTERNATIONAL IMMUNOPHARMACOLOGY
  • Wu, X
  • ,
  • A Yoshida
  • ,
  • T Sasano
  • ,
  • Y Iwakura
  • ,
  • Y Endo

4
4
開始ページ
513
終了ページ
520
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.1016/j.intimp.2003.10.011
出版者・発行元
ELSEVIER SCIENCE BV

Histamine modulates immune responses. There are at least two ways histamine might be supplied: one is its release from cells that pool pre-formed histamine and the other is its de novo formation via induction of histidine decarboxylase (HDC). Lipopolysaccharide (LPS) and the proinflammatory cytokine interleukin (IL)-1 induce a marked elevation of HDC activity in various tissues or organs. To examine the contribution of mast cells to HDC induction in mice given LPS or IL-1, we examined the effects of LPS and IL-1 on HDC activity and/or histamine content in various organs (liver, lung, spleen or bone marrow) in mast cell-deficient mice (W/W-v), their normal littermates (+/+) and BALB/c mice deficient in IL-1alpha, IL-1beta and tumor necrosis factor (TNF)-alpha (IL-1alphabeta/TNFalphaKO mice). In non-stimulated mice, the histamine in the lung and spleen was contained largely within mast cells. The LPS-stimulated increase in HDC activity in a given organ was similar between +/+ and W/W-v mice, and between IL-1alphabeta/TNFalphaKO BALB/c and control BALB/c mice, and led to increases in histamine. In W/Wv and +/+ mice, IL-1alpha also elevated HDC activity. These results suggest that (i) in liver, lung and spleen, either the major cells supplying histamine via HDC induction in response to LPS and IL-1 are not mast cells, or mast cells are not a prerequisite for the induction of HDC; (ii) the cells in which HDC is induced by LPS and IL-1 are similar or identical in a given organ; and (iii) neither IL-1 nor TNF-alpha is a prerequisite for the induction of HDC by LPS. (C) 2004 Elsevier B.V All rights reserved.

Web of Science ® 被引用回数 : 29

リンク情報
DOI
https://doi.org/10.1016/j.intimp.2003.10.011
Web of Science
https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000221282000003&DestApp=WOS_CPL

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