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The diacylated lipopeptide FSL-1 enhances phagocytosis of bacteria by macrophages through Toll-like receptor 2-mediated signaling pathway
Title: | The diacylated lipopeptide FSL-1 enhances phagocytosis of bacteria by macrophages through Toll-like receptor 2-mediated signaling pathway |
Authors: | Mae, Masako Browse this author | Iyori, Mitsuhiro Browse this author | Yasuda, Motoaki Browse this author | Shamsul, Haque Browse this author | Kataoka, Hideo Browse this author | Kiura, Kazuto Browse this author | Hasebe, Akira Browse this author | Totsuka, Yasunori Browse this author | Shibata, Ken-ichiro Browse this author →KAKEN DB |
Keywords: | Toll-like receptor 2 | the lipopeptide FSL-1 | phagocytosis | macrophage |
Issue Date: | 22-Feb-2007 |
Publisher: | Blackwell |
Journal Title: | FEMS immunology and medical microbiology |
Volume: | 49 |
Start Page: | 398 |
End Page: | 409 |
Publisher DOI: | 10.1111/j.1574-695X.2007.00218.x |
PMID: | 17316370 |
Abstract: | Enormous lines of evidence have been accumulated that Toll-like receptors (TLRs) function as sensors for microbial invasion. However, less is known about how signaling triggered by TLRs leads to phagocytosis of pathogens. This study was designed to determine whether stimulation of TLR2 with mainly the lipopeptide FSL-1 plays a role in phagocytosis of pathogens by macrophages. FSL-1 markedly enhanced phagocytosis of E. coli more strongly than that of S. aureus, but did not enhance phagocytosis of latex beads. FSL-1 stimulation resulted in enhanced phagocytosis of bacteria by macrophages from TLR2+/+mice but not those from TLR2-/- mice. Chinese hamster ovary cells stably expressing TLR2 failed tophagocytose these bacteria, but the cells expressing CD14 did. FSL-1 induced upregulation of the expression of phagocytic receptors including MSR1, CD36, DC-SIGN and Dectin-1 in THP-1 cells.Human embryonic kidney 293 cells transfected with DC-SIGN and MSR1 phagocytosed these bacteria. These results suggest that the FSL-1-induced enhancement of phagocytosis of bacteria by acrophages may be explained partially by the upregulation of scavenger receptors and the C-type lectins through TLR2-mediated signaling pathways and that TLR2 by itself does not function as a phagocytic receptor. |
Type: | article (author version) |
URI: | http://hdl.handle.net/2115/43975 |
Appears in Collections: | 歯学院・歯学研究院 (Graduate School of Dental Medicine / Faculty of Dental Medicine) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)
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Submitter: 柴田 健一郎
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