phosphodiesterase 4 inhibition but not beta-adrenergic stimulation suppresses tumor necrosis factor-alpha release in peripheral blood mononuclear cells in septic shock磷酸二酯酶4抑制但不是该项刺激抑制肿瘤坏死因子-α在外周血单核细胞在感染性休克.pdfVIP

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phosphodiesterase 4 inhibition but not beta-adrenergic stimulation suppresses tumor necrosis factor-alpha release in peripheral blood mononuclear cells in septic shock磷酸二酯酶4抑制但不是该项刺激抑制肿瘤坏死因子-α在外周血单核细胞在感染性休克.pdf

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phosphodiesterase 4 inhibition but not beta-adrenergic stimulation suppresses tumor necrosis factor-alpha release in peripheral blood mononuclear cells in septic shock磷酸二酯酶4抑制但不是该项刺激抑制肿瘤坏死因子-α在外周血单核细胞在感染性休克

Available online /content/12/6/R159 Vol 12 No 6 Open Access Research Phosphodiesterase 4 inhibition but not beta-adrenergic stimulation suppresses tumor necrosis factor-alpha release in peripheral blood mononuclear cells in septic shock Andreas Link, Simina Selejan, Christoph Maack, Monika Lenz and Michael Böhm Klinik für Innere Medizin III, Universität des Saarlandes, 66421 Homburg/Saar, Germany Corresponding author: Andreas Link, link@med-in.uni-saarland.de Received: 22 Sep 2008 Revisions requested: 20 Oct 2008 Revisions received: 19 Nov 2008 Accepted: 17 Dec 2008 Published: 17 Dec 2008 Critical Care 2008, 12:R159 (doi:10.1186/cc7158) This article is online at: /content/12/6/R159 © 2008 Link et al.; licensee BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License (/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Abstract Introduction Stimulation of beta -adrenergic receptors (β - Results Investigations were done by LPS (100 ng/mL) or SEB 2 2 ARs) inhibits tumor necrosis factor-alpha (TNF-α) release in (10 ng/mL) when TLR4 and TLR2 were maximally expressed. monocytes. In septic shock, endogenous catecholamines LPS- or SEB-treated CD14+ monocytes of healthy volunteers induce β2-AR downregulation, leading to an increased TNF-α were able to produce TNF-α. This effect was attenuated by release. The aims of this study were to analyze the molecular isoprenaline, forskolin, or rolipram in