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INFLAMMATION AND IMMUNOPHARMACOLOGY

Histamine Inhibits Lipopolysaccharide-Induced Tumor Necrosis Factor- Production in an Intercellular Adhesion Molecule-1- and B7.1-Dependent Manner

Departments of Tumour Biology (T.M., H.K.T., H.I., R.T., N.T.), Pharmacology (H.K.T., M.Y., S.M., M.N.), and Pathology (T.Y., T.A.), Okayama University Graduate School of Medicine and Dentistry, Okayama, Japan

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)- 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- 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- production induced by LPS. The modulatory effects of histamine on ICAM-1 and B7.1 expression and TNF- 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- production through the regulation of ICAM-1 and B7.1 expression, leading to the reduction of innate immune response stimulated by LPS.

Address correspondence to: Dr. Masahiro Nishibori, Department of Pharmacology, Okayama University Graduate School of Medicine and Dentistry, 2-5-1 Shikata-cho, Okayama 700-8558, Japan. E-mail: mbori{at}md.okayama-u.ac.jp

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