Phosphodiesterase 4B is essential for lipopolysaccharide-induced CC chemokine ligand 3 production in mouse macrophages

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題名:	Phosphodiesterase 4B is essential for lipopolysaccharide-induced CC chemokine ligand 3 production in mouse macrophages
作者:	金秀蓮;Lai, Ciou-Rong;Lo, Huan-Chu;Chen, Yi-Ling;Yang, Jing-Xing;Ding, Shiau-Li;Hsu, Hsian-He;Conti, Marco;Wu, Chin-Pyng;Jin, S.-L. Catherine
貢獻者:	生醫理工學院生命科學系
關鍵詞:	Analysis;Care and treatment;CC chemokine ligand 3;Gel electrophoresis;Health aspects;lipopolysaccharide;macrophage;macrophage infl ammatory protein-1α;macrophage inflammatory protein-1α;MEDLINE;Phosphodiesterase 4B;Phosphodiesterases;Scopus;T cells;Tumor necrosis factor
日期:	2015-01-01
上傳時間:	2026-04-23 11:13:37 (UTC+8)
出版者:	Wolters Kluwer Medknow Publications;台灣: 國防醫學大學
摘要:	摘要： Phosphodiesterase 4 (PDE4) inhibitors negatively modulate many infl ammatory responses, and some of these pharmacological effects are mediated by inhibition of PDE4B in infl ammatory cells. While inactivation of PDE4B, but not other PDE4 isotypes, is known to inhibit lipopolysaccharide (LPS)-induced tumor necrosis factor-α (TNF-α) production in macrophages, a cell type critical in mediating innate immunity, the impact of PDE4B on many other infl ammatory responses in these cells remains largely unknown. Materials and Methods: To investigate whether PDE4B regulates additional infl ammatory mediators other than TNF-α, in this study we initially used two-dimensional gel electrophoresis approach to screen the secreted proteins that are modulated by the PDE4 inhibitor rolipram in LPS-stimulated Raw 264.7 macrophages. Results: Three proteins were identifi ed, of which the proinfl ammatory chemokine CC chemokine ligand 3 (CCL3) and cytokine TNF-α were downregulated and the antiinfl ammatory cytokine interleukin-1 receptor antagonist was upregulated. Further analysis on CCL3 production in mouse peritoneal macrophages revealed that the reduced CCL3 secretion was associated with a substantial decrease in CCL3 mRNA accumulation. The inhibitory effect of rolipram on CCL3 production was mimicked by the protein kinase A activator 6-Bnz-cAMP, but not the exchange protein directly activated by cAMP activator 8-pCPT-2’-O-Me-cAMP. Analysis of PDE4-defi cient macrophages showed that ablation of only PDE4B reproduced the rolipram effect on CCL3 production. Moreover, PDE4 inhibitor potentially attenuates T-cell migration to CCL3 in infl ammatory sites. Conclusions: These fi ndings suggest that PDE4B may regulate the production of diverse infl ammatory mediators in LPS-stimulated macrophages, and an inhibitor with PDE4B selectivity should retain the anti-infl ammatory effects of nonselective PDE4 inhibitors in endotoxin-induced infl ammatory conditions. 出版者：台灣: 國防醫學大學出版日期： 2015-05-01 出處： Journal of Medical Sciences, 2015-05, Vol.35 (3), p.111-119 資源來源： Journals學術期刊資料庫(原CEPS) 版權： COPYRIGHT 2015 Medknow Publications and Media Pvt. Ltd. 識別號： ISSN: 1011-4564 識別號： ISSN: 2542-4939 識別號： DOI: 10.4103/1011-4564.158674
顯示於類別:	[生命科學系] 期刊論文

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