Histamine inhibits lipopolysaccharide-induced tumor necrosis factor-α production in an intercellular adhesion molecule-1- and B7.1-dependent manner

Toshihiko Morichika, Hideo Kohka Takahashi, Hiromi Iwagaki, Tadashi Yoshino, Ryuji Tamura, Minori Yokoyama, Shuji Mori, Tadaatsu Akagi, Masahiro Nishibori, Noriaki Tanaka

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Abstract

Lipopolysaccharide (LPS) is recognized as a key molecule in the pathogenesis of Gram negative sepsis and septic shock. In the present study, we demonstrate that LPS (1-1000 pg/ml) concentration dependently up-regulated the expression of intercellular adhesion molecule (ICAM)-1 B7.1, and B7.2 on human monocytes using fluorescence-activated cell sorting analysis, and that tumor necrosis factor (TNF)-α production induced by LPS in peripheral blood mononuclear cells (PBMCs) was inhibited by the addition of antibodies against these adhesion molecules, suggesting the dependence of TNF-α production on cell-cell interaction through these adhesion molecules. Moreover, we found that histamine (10-7-10-4 M) concentration dependently inhibited the expression of ICAM-1 and B7.1, but not B7.2 on monocytes induced by LPS. Histamine also inhibited the responses of TNF-α production induced by LPS. The modulatory effects of histamine on ICAM-1 and B7.1 expression and TNF-α 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-, H3-, and H4-receptor agonists, indicating the involvement of H2-receptors in the histamine action. Dibutyryl cAMP down-regulated ICAM-1 and B7.1 expression on monocytes stimulated by LPS, suggesting the mediation by the cyclic adenosine monophosphate-protein kinase A pathway of H2-receptor activation. These results as a whole indicated that histamine via H2-receptor inhibited the LPS-induced TNF-α production through the regulation of ICAM-1 and B7.1 expression, leading to the reduction of innate immune response stimulated by LPS.

Original languageEnglish
Pages (from-to)624-633
Number of pages10
JournalJournal of Pharmacology and Experimental Therapeutics
Volume304
Issue number2
DOIs
Publication statusPublished - Feb 1 2003

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Intercellular Adhesion Molecule-1
Histamine
Lipopolysaccharides
Tumor Necrosis Factor-alpha
Histamine H2 Receptors
Monocytes
thioperamide
Histamine H3 Receptors
Histamine Agonists
Chlorpheniramine
Famotidine
Septic Shock
Cyclic AMP-Dependent Protein Kinases
Innate Immunity
Cell Communication
Cyclic AMP
Blood Cells
Sepsis
Flow Cytometry
Antibodies

ASJC Scopus subject areas

  • Pharmacology

Cite this

Histamine inhibits lipopolysaccharide-induced tumor necrosis factor-α production in an intercellular adhesion molecule-1- and B7.1-dependent manner. / Morichika, Toshihiko; Takahashi, Hideo Kohka; Iwagaki, Hiromi; Yoshino, Tadashi; Tamura, Ryuji; Yokoyama, Minori; Mori, Shuji; Akagi, Tadaatsu; Nishibori, Masahiro; Tanaka, Noriaki.

In: Journal of Pharmacology and Experimental Therapeutics, Vol. 304, No. 2, 01.02.2003, p. 624-633.

Research output: Contribution to journalArticle

Morichika, Toshihiko ; Takahashi, Hideo Kohka ; Iwagaki, Hiromi ; Yoshino, Tadashi ; Tamura, Ryuji ; Yokoyama, Minori ; Mori, Shuji ; Akagi, Tadaatsu ; Nishibori, Masahiro ; Tanaka, Noriaki. / Histamine inhibits lipopolysaccharide-induced tumor necrosis factor-α production in an intercellular adhesion molecule-1- and B7.1-dependent manner. In: Journal of Pharmacology and Experimental Therapeutics. 2003 ; Vol. 304, No. 2. pp. 624-633.
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AU - Yokoyama, Minori

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AU - Nishibori, Masahiro

AU - Tanaka, Noriaki

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