Cutting edge: Expression patterns of surface and soluble triggering receptor expressed on myeloid cells-1 in human endotoxemia
Cutting edge: Expression patterns of surface and soluble triggering receptor expressed on myeloid cells-1 in human endotoxemia
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DOI：
10.4049/jimmunol.173.12.7131
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发表时间：
2004-12-15
影响因子：
4.4
通讯作者：
van der Poll, T
中科院分区：
文献类型：
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作者：
Knapp, S;Gibot, S;van der Poll, T
髓样细胞表达触发受体-1（TREM-1）是最近发现的一种参与炎症反应放大的分子。为了确定TREM-1的调节，我们研究了健康人体内和体外静脉内LPS攻击后的TREM-1表达和可溶性TREM-1血浆水平。粒细胞TREM-1表达在基线时高，并且在LPS暴露后立即下调，沿着可溶性TREM-1增加。单核细胞在体内和体外LPS后显示TREM-1的逐渐上调。体外研究将这些发现扩展到高度纯化的脂磷壁酸和肺炎链球菌。非细菌TLR配体如聚肌苷-聚胞苷酸和咪唑并喹啉以及TLR 9配体CpG不影响TREM-1表达。LPS诱导的TREM-1表面表达的改变不是TNF-α或IL-10增加的结果。抑制剂研究揭示了LPS诱导的单核细胞上TREM-1上调中的PI 3 K依赖性途径，而MAPK发挥有限的作用。
Triggering receptor expressed on myreloid cells-1 (TREM-1) is a recently identified molecule involved in the amplification of inflammation. To determine the regulation of TREM-1, we studied TREM-1 expression and soluble TREM-1 plasma levels upon i.v. LPS challenge in healthy humans in vivo and in vitro. Granulocyte TREM-1 expression was high at baseline and immediately down-regulated upon LPS exposure along with an increase in soluble TREM-1. Monocytes displayed a gradual up-regulation of TREM-1 upon LPS in vivo and in vitro. In vitro studies extended these findings to highly purified lipoteichoic acid and Streptococcus pneumoniae. Non-bacterial TLR ligands such as polyinosine-polycytidylic acid and imidazoquinoline, as well as the TLR9 ligand CpG, did not impact TREM-1 expression. The LPS-induced alterations in TREM-1 surface expression were not a result of increased TNF-alpha or IL-10. Inhibitor studies disclosed a PI3K-dependent pathway in LPS-induced upregulation of TREM-1 on monocytes, whereas MAPK played a limited role.