The diacylated lipopeptide FSL-1 enhances phagocytosis of bacteria by macrophages through a Toll-like receptor 2-mediated signalling pathway
The diacylated lipopeptide FSL-1 enhances phagocytosis of bacteria by macrophages through a Toll-like receptor 2-mediated signalling pathway
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DOI：
10.1111/j.1574-695x.2007.00218.x
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发表时间：
2007-04-01
影响因子：
--
通讯作者：
Shibata, Ken-ichiro
中科院分区：
文献类型：
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作者：
Mae, Masako;Iyori, Mitsuhiro;Shibata, Ken-ichiro
大量证据表明toll样受体（TLRs）是微生物入侵的传感器。然而，对于tlr触发的信号如何导致病原体的吞噬，我们知之甚少。本研究旨在确定主要以脂肽FSL-1刺激TLR2是否在巨噬细胞吞噬病原体中起作用。FSL-1对大肠杆菌的吞噬作用明显大于对金黄色葡萄球菌的吞噬作用，但对乳胶珠的吞噬作用没有增强作用。FSL-1刺激可增强TLR2（+/+）小鼠巨噬细胞对细菌的吞噬作用，而TLR2（-/-）小鼠则无此作用。稳定表达TLR2的中国仓鼠卵巢细胞不能吞噬这些细菌，而表达CD14的细胞可以。FSL-1诱导THP-1细胞中吞噬受体的表达上调，包括MSR1、CD36、DC-SIGN和Dectin-1。转染DC-SIGN和MSR1的人胚胎肾293细胞能够吞噬这些细菌。这些结果表明，fsl -1诱导的巨噬细胞对细菌吞噬能力的增强可能部分解释为通过TLR2介导的信号通路上调清道夫受体和c型凝集素，而TLR2本身并不作为吞噬受体。
A significant amount of evidence has been accumulated to show that Toll-like receptors (TLRs) function as sensors for microbial invasion. However, little is known about how signalling triggered by TLRs leads to the phagocytosis of pathogens. This study was designed to determine whether stimulation of TLR2 mainly with the lipopeptide FSL-1 plays a role in the phagocytosis of pathogens by macrophages. FSL-1 enhanced the phagocytosis of Escherichia coli to a markedly greater extent than it did that of Staphylococcus aureus, but did not enhance the phagocytosis of latex beads. FSL-1 stimulation resulted in enhanced phagocytosis of bacteria by macrophages from TLR2(+/+) mice but not by those from TLR2(-/-) mice. Chinese hamster ovary cells stably expressing TLR2 failed to phagocytose 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 macrophages may be explained partly by the upregulation of scavenger receptors and the C-type lectins through TLR2-mediated signalling pathways, and that TLR2 by itself does not function as a phagocytic receptor.