Rui Yamaguchi
Department Kumamoto Health Science University Department of Medical Technology, Faculty of Health Science Kumamoto Health Science University Graduate School Division of Health Sciences, Graduate School of Health Sciences Position Associate Professor |
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Language | English |
Publication Date | 2015/06 |
Type | |
Peer Review | Peer reviewed |
Title | Mechanism of interleukin-13 production by granulocyte-macrophage colony-stimulating factor-dependent macrophages via protease-activated receptor-2 |
Contribution Type | |
Journal | Blood Cells Mol Dis. |
Journal Type | Another Country |
Volume, Issue, Page | 55,pp.21-26 |
Total page number | 5 |
Authorship | Lead author |
Author and coauthor | Yamaguchi R, Yamamoto T, Sakamoto A, Ishimaru Y, Narahara S, Sugiuchi H, Hirose E, Yamaguchi Y |
Details | Background: Granulocyte-macrophage colony-stimulating factor (GM-CSF) promotes classically activated M1 macrophages. GM-CSF upregulates protease-activated receptor-2 (PAR-2) protein expression and activation of PAR-2 by human neutrophil elastase (HNE) regulates cytokine production.
PAR-2 protein was detected in GM-CSF-dependent macrophages by Western blotting. Unexpectedly, PD98059 (an ERK1 inhibitor) increased IL-13 production, even at higher concentrations. Interestingly, U0126 (an ERK1/2 inhibitor) reduced IL-13 production in a concentration-dependent manner. Neither SB203580 (a p38alpha/p38beta inhibitor) nor BIRB796 (a p38gamma/p38delta inhibitor) affected IL-13 production, while TMB-8 (a calcium chelator) diminished IL-13 production.Stimulation with HNE promoted the production of IL-13 (a Th2 cytokine) by GM-CSF-dependent M1 macrophages. PAR-2-mediated IL-13 production may be dependent on the Ca(2+)/ERK2 signaling pathway. |