CD14-dependent lipopolysaccharide-induced ß-defensin-2 expression in human tracheobronchial epithelium
CD14-dependent lipopolysaccharide-induced ß-defensin-2 expression in human tracheobronchial epithelium
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DOI：
10.1074/jbc.m000184200
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发表时间：
2000-09-22
影响因子：
4.8
通讯作者：
Randell, SH
中科院分区：
文献类型：
--
作者：
Becker, MN;Diamond, G;Randell, SH
在病原体组分与模式识别受体如CD 14和Toll样受体（TLR）结合后诱导宿主抗微生物分子是先天免疫的关键特征。人气道上皮是一个重要的环境界面，但LPS识别途径尚未确定。我们假设LPS会通过CD 14依赖性机制触发人气管支气管上皮细胞（hTBE）中的β-防御素（hBD 2）mRNA，最终激活NF-κ B B。LPS刺激hTBE细胞后24 h，hBD 2 mRNA平均增加3倍。我们首次证明了hTBE细胞中存在CD 14 mRNA和细胞表面蛋白，并表明CD 14中和作用可消除LPS对hBD 2 mRNA的诱导作用。此外，我们证明了TLR mRNA在hTBE细胞和NF-κ B B激活后LPS。因此，hTBE细胞中hBD 2的LPS诱导需要CD 14，其可与TLR复合以最终激活NF-κ B。
The induction of host antimicrobial molecules following binding of pathogen components to pattern recognition receptors such as CD14 and the Toll-like receptors (TLRs) is a key feature of innate immunity. The human airway epithelium is an important environmental interface, but LPS recognition pathways have not been determined. We hypothesized that LPS would trigger beta-defensin (hBD2) mRNA in human tracheobronchial epithelial (hTBE) cells through a CD14-dependent mechanism, ultimately activating NF-kappa B. An average 3-fold increase in hBD2 mRNA occurs 24 h after LPS challenge of hTBE cells. For the first time, we demonstrate the presence of CD14 mRNA and cell surface protein in hTBE cells and show that CD14 neutralization abolishes LPS induction of hBD2 mRNA. Furthermore, we demonstrate TLR mRNA in hTBE cells and NF-kappa B activation following LPS. Thus, LPS induction of hBD2 in hTBE cells requires CD14, which may complex with a TLR to ultimately activate NF-kappa B.