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The diacylated lipopeptide FSL-1 enhances phagocytosis of bacteria by macrophages through Toll-like receptor 2-mediated signaling pathway

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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)

Submitter: 柴田 健一郎

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