Effects of Escherichia coli and E. coli lipopolysaccharides on the function of human ureteral epithelial cells cultured in serum-free medium.
Effects of Escherichia coli and E. coli lipopolysaccharides on the function of human ureteral epithelial cells cultured in serum-free medium.
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大肠杆菌和大肠杆菌脂多糖对无血清培养基培养的人输尿管上皮细胞功能的影响。
DOI：
10.1128/iai.61.8.3304-3312.1993
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发表时间：
1993
影响因子：
3.1
通讯作者：
Elgavish,A
中科院分区：
文献类型：
--
作者：
Elgavish,A
大肠杆菌是最常从人类泌尿道感染中分离出来的微生物。其他人的早期研究表明，细菌附着和毒素的产生（例如，脂多糖[LPS]）增强白细胞向感染部位的募集和粘膜炎症。这些变化发生的机制尚未完全确定。在本研究中，从人输尿管分离的上皮细胞培养物（UT细胞）（A. Elgavish，J. J. Wille，F. Rahemtulla和L.德布罗，阿姆。J.Physiol.261：C916-C926，1991; J.J. Wille，J. Park和A. Elgavish，J. Cell. Physiol.150：52-58，1992）用作模型系统，用其探索大肠杆菌和大肠杆菌的作用机制。coliLPS诱导的UT细胞凋亡。E.大肠杆菌粘附到UT细胞，并抑制载体介导的硫酸盐摄取的一半，在未经处理的UT细胞，这表明可用于硫酸化的细胞内池可能是较低的感染细胞，并可能导致生产的硫酸化不足的糖缀合物。将UT细胞与E. coli LPS抑制载体介导的硫酸盐摄取的程度与全大肠杆菌相似。大肠杆菌中，E.大肠杆菌对硫酸盐摄取的影响可能是由LPS介导的。LPS引起快速增殖的UT细胞中Na+含量增加，但在静止细胞中不增加。我们假设细胞内离子环境的这种变化或与之相关的变化（例如，pH或Ca 2+水平）可以充当转导信号。LPS刺激ICAM-1在快速增殖但不静止的UT细胞的细胞表面上聚集的事实支持了这种可能性。这项研究表明，在体内，LPS刺激ICAM-1的表面上的尿路上皮细胞簇可能允许更有效的白细胞结合。这可能是早期体内研究结果的基础机制，表明LPS在尿路感染后将白细胞募集到尿路中作为宿主防御机制的作用。
Escherichia coli is the microorganism most commonly isolated from human urinary tract infections. Earlier studies by others have shown that bacterial attachment and production of toxins (e.g., lipopolysaccharides [LPS]) enhance recruitment of leukocytes to the infection site and mucosal inflammation. The mechanisms by which these changes occur have not been completely defined. In the present study, epithelial cell cultures isolated from the human ureter (UT cells) (A. Elgavish, J. J. Wille, F. Rahemtulla, and L. Debro, Am. J. Physiol. 261:C916-C926, 1991; J. J. Wille, J. Park, and A. Elgavish, J. Cell. Physiol. 150:52-58, 1992) served as a model system with which to explore the mechanisms of action of Escherichia coli and E. coli LPS in UT cells. E. coli adhered to UT cells and inhibited carrier-mediated sulfate uptake to half of that in untreated UT cells, suggesting that the intracellular pool of sulfate available for sulfation may be lower in infected cells and may lead to the production of undersulfated glycoconjugates. Incubation of UT cells with E. coli LPS inhibited carrier-mediated sulfate uptake to an extent similar to that caused by whole E. coli, indicating that the effect of E. coli on sulfate uptake may be mediated by LPS. LPS caused an increase in Na+ content in rapidly proliferating UT cells but not in quiescent cells. We postulated that this change in the intracellular ionic environment or changes coupled to it (e.g., pH or Ca2+ levels) may serve as a transducing signal. This possibility was supported by the fact that LPS stimulated clustering of ICAM-1 on the cell surface of rapidly proliferating but not quiescent UT cells. This study suggests that, in vivo, LPS stimulation of ICAM-1 clustering on the surface of the urothelium may allow more effective binding of leukocytes. This may be the mechanism underlying earlier findings in vivo indicating a role for LPS in the recruitment of leukocytes to the urinary tract as a host defense mechanism following urinary tract infection.
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DOI：
10.1111/j.1748-1716.1972.tb05166.x
发表时间：
1972-01-01
期刊：
ACTA PHYSIOLOGICA SCANDINAVICA
影响因子：
--
作者：
HAGLUND, U;LUNDGREN, O
通讯作者：
LUNDGREN, O
影响因子：
--
作者：
PARKS, DA;GRANGER, DN
通讯作者：
GRANGER, DN
影响因子：
29.4
作者：
D. Granger;J. Barrowman
通讯作者：
J. Barrowman
白三烯 C4 和 D4 对豚鼠皮肤微血管的影响。
DOI：
--
发表时间：
1981
期刊：
Prostaglandins
影响因子：
--
作者：
M. Peck;P. Piper;T. Williams
通讯作者：
T. Williams
DOI：
10.1016/0005-2760(86)90145-1
发表时间：
1986-09-12
期刊：
BIOCHIMICA ET BIOPHYSICA ACTA
影响因子：
--
作者：
DREYLING, KW;HOPPE, U;PESKAR, BM
通讯作者：
PESKAR, BM