Abstract
In the previous study, we demonstrated that interleukin (IL)-18 up-regulated intercellular adhesion molecule-1 (ICAM-1) expression on monocytes in human peripheral blood mononuclear cells (PBMC) and that heterotypic interaction between monocytes/T or NK cells through ICAM-1/LFA-1 intensified the production of IL-12, interferon-γ (IFN-γ), and tumor necrosis factor-α (TNF-α) in PBMC. In the present study, we demonstrate that histamine inhibited the ICAM-1 expression in monocytes induced by IL-18 using flow cytometry and that the responses of IL-12, IFN-γ, and TNF-α induced by IL-18 were concentration dependently inhibited by coexisting histamine, whereas IL-18-inhibited IL-10 production was reversed by the same concentrations of histamine. The modulatory effects of histamine on ICAM-1 expression and cytokine production were all concentration dependently antagonized by famotidine but not by d-chlorpheniramine and thioperamide, and were mimicked by selective H2-receptor agonists but not by H1- and H3-receptor agonists, indicating the involvement of H2-receptors in histamine action. The inhibition of IL-18-induced IFN-γ by histamine was ascribed to the strong inhibition of IL-12 production by histamine. Histamine thus operates the negative feedback mechanism against IL-18-activated cytokine cascade through the strong inhibitory effect on ICAM-1 expression and IL-12 production in monocytes, contributing to the formation of diverse pattern of cytokine activation from Th1 to Th2, depending on the monocyte/macrophage activation and cytokine environment.
| Original language | English |
|---|---|
| Pages (from-to) | 227-235 |
| Number of pages | 9 |
| Journal | Journal of Pharmacology and Experimental Therapeutics |
| Volume | 300 |
| Issue number | 1 |
| DOIs | |
| Publication status | Published - 2002 |
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ASJC Scopus subject areas
- Pharmacology
Cite this
Histamine regulation of interleukin-18-initiating cytokine cascade is associated with down-regulation of intercellular adhesion molecule-1 expression in human peripheral blood mononuclear cells. / Takahashi, Hideo Kohka; Yoshida, Atsushi; Iwagaki, Hiromi; Yoshino, Tadashi; Itoh, Hideyuki; Morichika, Toshihiko; Yokoyama, Minori; Akagi, Tadaatsu; Tanaka, Noriaki; Mori, Shuji; Nishibori, Masahiro.
In: Journal of Pharmacology and Experimental Therapeutics, Vol. 300, No. 1, 2002, p. 227-235.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Histamine regulation of interleukin-18-initiating cytokine cascade is associated with down-regulation of intercellular adhesion molecule-1 expression in human peripheral blood mononuclear cells
AU - Takahashi, Hideo Kohka
AU - Yoshida, Atsushi
AU - Iwagaki, Hiromi
AU - Yoshino, Tadashi
AU - Itoh, Hideyuki
AU - Morichika, Toshihiko
AU - Yokoyama, Minori
AU - Akagi, Tadaatsu
AU - Tanaka, Noriaki
AU - Mori, Shuji
AU - Nishibori, Masahiro
PY - 2002
Y1 - 2002
N2 - In the previous study, we demonstrated that interleukin (IL)-18 up-regulated intercellular adhesion molecule-1 (ICAM-1) expression on monocytes in human peripheral blood mononuclear cells (PBMC) and that heterotypic interaction between monocytes/T or NK cells through ICAM-1/LFA-1 intensified the production of IL-12, interferon-γ (IFN-γ), and tumor necrosis factor-α (TNF-α) in PBMC. In the present study, we demonstrate that histamine inhibited the ICAM-1 expression in monocytes induced by IL-18 using flow cytometry and that the responses of IL-12, IFN-γ, and TNF-α induced by IL-18 were concentration dependently inhibited by coexisting histamine, whereas IL-18-inhibited IL-10 production was reversed by the same concentrations of histamine. The modulatory effects of histamine on ICAM-1 expression and cytokine production were all concentration dependently antagonized by famotidine but not by d-chlorpheniramine and thioperamide, and were mimicked by selective H2-receptor agonists but not by H1- and H3-receptor agonists, indicating the involvement of H2-receptors in histamine action. The inhibition of IL-18-induced IFN-γ by histamine was ascribed to the strong inhibition of IL-12 production by histamine. Histamine thus operates the negative feedback mechanism against IL-18-activated cytokine cascade through the strong inhibitory effect on ICAM-1 expression and IL-12 production in monocytes, contributing to the formation of diverse pattern of cytokine activation from Th1 to Th2, depending on the monocyte/macrophage activation and cytokine environment.
AB - In the previous study, we demonstrated that interleukin (IL)-18 up-regulated intercellular adhesion molecule-1 (ICAM-1) expression on monocytes in human peripheral blood mononuclear cells (PBMC) and that heterotypic interaction between monocytes/T or NK cells through ICAM-1/LFA-1 intensified the production of IL-12, interferon-γ (IFN-γ), and tumor necrosis factor-α (TNF-α) in PBMC. In the present study, we demonstrate that histamine inhibited the ICAM-1 expression in monocytes induced by IL-18 using flow cytometry and that the responses of IL-12, IFN-γ, and TNF-α induced by IL-18 were concentration dependently inhibited by coexisting histamine, whereas IL-18-inhibited IL-10 production was reversed by the same concentrations of histamine. The modulatory effects of histamine on ICAM-1 expression and cytokine production were all concentration dependently antagonized by famotidine but not by d-chlorpheniramine and thioperamide, and were mimicked by selective H2-receptor agonists but not by H1- and H3-receptor agonists, indicating the involvement of H2-receptors in histamine action. The inhibition of IL-18-induced IFN-γ by histamine was ascribed to the strong inhibition of IL-12 production by histamine. Histamine thus operates the negative feedback mechanism against IL-18-activated cytokine cascade through the strong inhibitory effect on ICAM-1 expression and IL-12 production in monocytes, contributing to the formation of diverse pattern of cytokine activation from Th1 to Th2, depending on the monocyte/macrophage activation and cytokine environment.
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UR - http://www.scopus.com/inward/citedby.url?scp=18244405367&partnerID=8YFLogxK
U2 - 10.1124/jpet.300.1.227
DO - 10.1124/jpet.300.1.227
M3 - Article
C2 - 11752121
AN - SCOPUS:18244405367
VL - 300
SP - 227
EP - 235
JO - Journal of Pharmacology and Experimental Therapeutics
JF - Journal of Pharmacology and Experimental Therapeutics
SN - 0022-3565
IS - 1
ER -