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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 | 2017/06 |
| Type | |
| Peer Review | Peer reviewed |
| Title | Surfactant protein D inhibits interleukin-12p40 production by macrophages through the SIRPα/ROCK/ERK signaling pathway |
| Contribution Type | |
| Journal | Am J Med Sci. |
| Journal Type | Another Country |
| Volume, Issue, Page | 353,pp.559-567 |
| Total page number | 8 |
| Authorship | Lead author |
| Author and coauthor | Yamaguchi R, Sakamoto A, Yamamoto T, Narahara S, Sugiuchi H, Yamaguchi Y |
| Details | Objective: Interleukin (IL)-12 has a pivotal profibrotic role in the development of idiopathic pulmonary fibrosis (IPF). Medical research trials based on IPF registry databases have actively recruited patients.
Results: GM-CSF was found to upregulate SIRPα expression by macrophages. PD98059 (an extracellular signal-regulated kinase [ERK] inhibitor) blunted induction of SIRPα expression by GM-CSF. SP-D significantly attenuated IL-12p40 production by macrophages after stimulation with LPS. Silencing of SIRPα/β/γ significantly reversed this inhibitory effect of SP-D. In contrast, neither SB023580 (a p38α/β MAPK inhibitor) nor BIRB796 (a p38γ/δ MAPK inhibitor) attenuated the inhibitory effect of SP-D on LPS-stimulated production of IL-12p40. Conclusions: These findings suggest that SP-D inhibits LPS-stimulated production of IL-12p40 via the SIRPα/ROCK/ERK signaling pathway. |