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Regulation by Interleukin-1β of Gene Expression of Bradykinin B1 Receptor in MH-S Murine Alveolar Macrophage Cell Line

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Abstract

The effects of recombinant murine interleukin (IL)-1β on gene expression of murine bradykinin B1 receptor (BDKRB1) in MH-S murine alveolar macrophage cell line were evaluated. BDKRB1 mRNA expression in MH-S cells was increased by IL-1β (1, 3, and 10 ng/ml) in a time-dependent manner, peaking at 3-4 h by 100-1000 fold. IL-1β (5 ng/ml, 24h) also induced significant binding to [3H]-des-Arg10-kallidin with a dissociation constant (Kd) of 2.95 nM and a maximal binding density (Bmax) of 670 sites/cell. Des-Arg10-kallidin (10 μM), a BDKRB1 agonist, increased intracellular calcium ion ([Ca2+]i) in IL-1β (5 ng/ml, 24 h)-exposed cells, an increase not observed in the cells not exposed to IL-1β. A significant increase of tumor necrosis factor (TNF)-α secretion occurred in the IL-1β (5 ng/ml, 24 h)-exposed cells following addition of des-Arg10-kallidin (the IL-1β-exposed group: 57. 8 ± 13.7 vs. the vehicle-exposed group: 16.7 ± 4.3 pg/ml, p < 0.05 after a 100 nM des-Arg10-kallidin for 8 h), with an optimal effect at 3-100 nM. These data suggest that IL-1β may up-regulate BDKRB1-mediated functions of alveolar macrophages via an induction of BDKRB1 gene expression.

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    To whom correspondence should be addressed at First Department of Internal Medicine, Gunma University School of Medicine, 3-39-15 Showa Maebashi, Gunma, 371-8511, Japan. Fax: 027-220-8136. E-mail: [email protected].

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