Quinine inhibits production of tumor necrosis factor-alpha from human alveolar macrophages.

N. Maruyama, Y. Kakuta, K. Yamauchi, Y. Ohkawara, T. Aizawa, T. Ohrui, M. Nara, T. Oshiro, I. Ohno, G. Tamura

研究成果: Article査読

36 被引用数 (Scopus)

抄録

Although tumor necrosis factor-alpha (TNF-alpha) produced by alveolar macrophages plays a key role in acute and chronic inflammatory states of the lung, the regulation of TNF-alpha synthesis remains to be elucidated. Recently, a K channel blocker, quinine, has been reported to inhibit cell proliferation and protein synthesis in lymphocytes, implicating physiologic roles for K channels in lymphocytes. The effect of quinine on protein synthesis in human alveolar macrophages, however, has not been determined, although alveolar macrophages have been reported to have two types of K channels. Therefore, we investigated the effect of quinine on TNF-alpha production from human alveolar macrophages. The production of TNF-alpha was induced by lipopolysaccharide (LPS) stimulation. We obtained the following results. First, LPS induced time-dependent activation of both types of K channels. Second, quinine inhibited TNF-alpha release in a dose-dependent fashion at concentrations of 50 to 200 microM, concentrations capable of blocking both types of K channels, with no appreciable reduction of phagocytosis of latex beads. Third, the compound remarkably inhibited the expression of TNF-alpha mRNA without any appreciable effect on the expression of beta-actin mRNA. These results indicate that both types of K channels are activated by stimulation with LPS and that quinine, at concentrations required to inhibit K channels, specifically blocks TNF-alpha production of human alveolar macrophages at the level of gene transcription.

本文言語English
ページ(範囲)514-520
ページ数7
ジャーナルAmerican journal of respiratory cell and molecular biology
10
5
DOI
出版ステータスPublished - 1994 5

ASJC Scopus subject areas

  • 分子生物学
  • 呼吸器内科
  • 臨床生化学
  • 細胞生物学

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