首页> 外文期刊>The Journal of Infectious Diseases >Lipopolysaccharide-binding protein increases toll-like receptor 4-dependent activation by nontypeable Haemophilus influenzae.
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Lipopolysaccharide-binding protein increases toll-like receptor 4-dependent activation by nontypeable Haemophilus influenzae.

机译:脂多糖结合蛋白通过不可分型的流感嗜血杆菌增加toll样受体4依赖性激活。

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Nontypeable Haemophilus influenzae (NTHi) is a common cause of respiratory tract infections. This study investigated the ability of NTHi to bind lipopolysaccharide-binding protein (LBP) derived from respiratory epithelial cells and the subsequent stimulation of transfected cells expressing membrane-bound CD14 and toll-like receptor 2 (TLR2) or TLR4. In the absence of LBP, NTHi at high concentrations (100 bacteria/epithelial cell) were required to induce signals through TLR2 and TLR4. Flow cytometry showed that NTHi in the stationary phase bound more LBP than did log-phase bacteria. Of interest, as few as 1 LBP-bearing bacterium/cell induced strong signaling through TLR4. In contrast, LBP bound to NTHi did not promote any increased signaling mediated by TLR2, compared with NTHi without LBP. These data suggest that, upon NTHi infection, low numbers of bacteria binding LBP may activate TLR4-bearing cells, such as alveolar macrophages, and consequently induce an inflammatory response.
机译:不可分型的流感嗜血杆菌(NTHi)是呼吸道感染的常见原因。这项研究调查了NTHi结合源自呼吸道上皮细胞的脂多糖结合蛋白(LBP)的能力,以及随后对表达膜结合CD14和Toll样受体2(TLR2)或TLR4的转染细胞的刺激作用。在没有LBP的情况下,需要高浓度的NTHi(100个细菌/上皮细胞)通过TLR2和TLR4诱导信号。流式细胞仪显示,与对数期细菌相比,固定相中的NTHi结合了更多的LBP。有趣的是,只有1个带有LBP的细菌/细胞通过TLR4诱导了强信号转导。相反,与没有LBP的NTHi相比,结合至NTHi的LBP没有促进由TLR2介导的任何增加的信号传导。这些数据表明,在NTHi感染后,少量细菌与LBP结合可能会激活带有TLR4的细胞(如肺泡巨噬细胞),从而引起炎症反应。

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