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首页> 外文期刊>Infection and immunity >Tumor necrosis factor induction by an aqueous phenol-extracted lipopolysaccharide complex from Bacteroides species.
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Tumor necrosis factor induction by an aqueous phenol-extracted lipopolysaccharide complex from Bacteroides species.

机译：来自拟杆菌属的水性苯酚提取的脂多糖复合物诱导肿瘤坏死因子。

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摘要

The stimulation of macrophages and monocytes by lipopolysaccharide (LPS) results in the secretion of tumor necrosis factor (TNF), a cytokine which is thought to play a pivotal role in subsequent host responses. Its induction is thought to be facilitated by the binding of complexes of LPS and LPS-binding protein to CD14. The LPS of Bacteroides species was considered a weak endotoxin; however, in a recent study we have shown that the biological activity and chemical composition of the LPS from Bacteroides species are dependent on the extraction method. The present study determines the capacity of LPS extracted by aqueous phenol (the method for producing an LPS of high endotoxic activity) from four species of Bacteroides to induce TNF. Induction was investigated from human mononuclear leukocytes (MNL), THP-1 cells (with and without enhancement by vitamin D2 for CD14), and peritoneal macrophages from C3H/HeJ (LPS nonresponder) and C3H/HeN (LPS responder) mice. Escherichia coli O18K- LPS, a typical smooth LPS of heterogeneous molecular mass, was used as a control throughout. The stimulation of TNF production by E. coli LPS was between two- and fourfold more than that by Bacteroides LPS in MNL, in THP-1 cells (with enhancement for CD14), and in peritoneal macrophages from C3H/HeN mice. In THP-1 cells (without enhancement for CD14), there was no significant difference in TNF production between E. coli and Bacteroides LPSs. In peritoneal macrophages from C3H/HeJ mice, E. coli LPS stimulated no TNF production, but there was no significant difference in TNF production from peritoneal macrophages from C3H/HeJ and C3H/HeN mice by Bacteroides LPS. In all cell populations, there was a peak of TNF production after approximately 4 h of stimulation with all LPSs tested. However, other peaks of TNF production were seen in MNL and THP-1 cells (with enhancement for CD14) after stimulation with E. coli LPS only. In stimulation assays in which Bacteroides LPS was together with but in excess of E. coli LPS, it was found that TNF production from MNL and THP-1 cells (with and without enhancement for CD14) was comparable to that of Bacteroides LPS alone and not E. coli LPS alone. An anti-CD14 monoclonal antibody did not inhibit Bacteroides LPS-stimulated TNF production. However, E. coli LPS-stimulated TNF release was inhibited by an anti-CD14 monoclonal antibody, most noticeably in MNL and THP-1 cells (with enhancement for CD14).(ABSTRACT TRUNCATED AT 400 WORDS)
机译：脂多糖（LPS）刺激巨噬细胞和单核细胞导致肿瘤坏死因子（TNF）的分泌，肿瘤坏死因子（TNF）是一种细胞因子，被认为在随后的宿主反应中起关键作用。 LPS和LPS结合蛋白的复合物与CD14的结合促进了其诱导。拟杆菌属的脂多糖被认为是一种弱内毒素。然而，在最近的研究中，我们已经证明了来自拟杆菌属物种的脂多糖的生物学活性和化学组成取决于提取方法。本研究确定了从四种拟杆菌属中提取的苯酚水溶液（生产具有高内毒素活性的LPS的方法）提取的LPS诱导TNF的能力。研究了人单核白细胞（MNL），THP-1细胞（对CD14有和没有维生素D2增强作用）以及C3H / HeJ（LPS无反应）和C3H / HeN（LPS反应）小鼠腹膜巨噬细胞的诱导作用。大肠杆菌O18K-LPS，一种典型的异质分子量的光滑LPS，始终用作对照。在MNL中，在THP-1细胞中（对CD14增强）和在C3H / HeN小鼠腹膜巨噬细胞中，大肠杆菌LPS对细菌产生的TNF的刺激作用比拟杆菌LPS对TNF的刺激高出两倍至四倍。在THP-1细胞（不增强CD14）中，大肠杆菌和拟杆菌LPS之间的TNF产生没有显着差异。在C3H / HeJ小鼠的腹膜巨噬细胞中，大肠杆菌LPS不会刺激TNF的产生，但是拟杆菌LPS的C3H / HeJ和C3H / HeN小鼠的腹膜巨噬细胞的TNF产生没有显着差异。在所有细胞群中，用所有测试的LPS刺激约4小时后，TNF产生峰值。但是，仅用大肠杆菌LPS刺激后，在MNL和THP-1细胞（CD14增强）中发现了TNF产生的其他峰值。在拟杆菌属LPS与但不超过大肠杆菌属LPS的刺激试验中，发现MNL和THP-1细胞的TNF产生（CD14增强或不增强）与单独的拟杆菌LPS相当，而与非细菌LPS相当。仅大肠杆菌LPS。抗CD14单克隆抗体不抑制拟杆菌LPS刺激的TNF产生。但是，大肠杆菌LPS刺激的TNF释放被抗CD14单克隆抗体抑制，最明显的是在MNL和THP-1细胞中（增强了CD14）。（摘要截短了400字）

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