Gamma interferon modulation of prostaglandin E2 release from monocytes stimulated with lipopolysaccharides from Bacteroides intermedius, Bacteroides gingivalis, and Salmonella typhimurium.
Gamma interferon modulation of prostaglandin E2 release from monocytes stimulated with lipopolysaccharides from Bacteroides intermedius, Bacteroides gingivalis, and Salmonella typhimurium.
复制标题
γ 干扰素调节来自中间拟杆菌、牙龈拟杆菌和鼠伤寒沙门氏菌的脂多糖刺激的单核细胞中前列腺素 E2 的释放。
DOI：
10.1111/j.1399-302x.1988.tb00099.x
复制
发表时间：
1988
影响因子：
--
通讯作者：
Nichols,FC
中科院分区：
文献类型：
--
作者：
Garrison,SW;Nichols,FC
通过热原性和骨吸收测定以及局部施瓦茨曼反应进行比较，来自拟杆菌属的脂多糖 (LPS) 的效力低于肠杆菌 LPS 制剂。在这项研究中，相对于相同剂量的鼠伤寒沙门氏菌LPS，检查了来自中间拟杆菌和牙龈拟杆菌的LPS制剂刺激人单核细胞释放PGE2的能力。此外，还对每种 LPS 制剂检查了重组γ干扰素 (IFN-γ) 增强 PGE2 释放的能力。通过逆流离心分离的单核细胞单独暴露于 LPS（1 ng/ml、100 ng/ml 和 10 ng/ml）或与 IFN-γ（10 单位/ml）组合。 PGE2 水平（通过 RIA 测量）是在以下孵育期内暴露的单核细胞培养物上清液中测定的：0-8、8-24、24-48 和 48-72 小时。用沙门氏菌 LPS 处理的单核细胞释放的 PGE2 量比用拟杆菌属 LPS 制剂处理的细胞多 2 至 3 倍。虽然单独使用 IFN-γ 不会刺激 PGE2 释放，但当单核细胞与 IFN-γ 同时培养时，拟杆菌引起的 PGE2 释放显着增加。沙门氏菌LPS引起的PGE2释放不受干扰素的显着影响。这些发现表明 IFN-γ 可以显着增强拟杆菌 LPS 刺激的单核细胞释放 PGE2。此外，观察到的这些 LPS 制剂相对于沙门氏菌 LPS 的弱点可以通过用 IFN-γ 共同处理单核细胞来很大程度上克服。
Lipopolysaccharides (LPS) fromBacteroidesspecies are less potent than enterobacterial LPS preparations when compared by pyrogenicity and bone resorption assays and by the localized Schwartzman reaction. In this investigation, LPS preparations fromBacteroides intermediusandBacteroides gingivaliswere examined for their capacity to stimulate PGE2 release from human monocytes relative to identical doses ofSalmonella typhimuriumLPS. In addition, the capacity of recombinant gamma interferon (IFN‐γ) to potentiate PGE2release was examined with each LPS preparation. Monocytes, separated by counter flow centrifugation, were exposed to LPS (1 ng/ml, 100 ng/ml and 10 ng/ml) alone or in combination with IFN‐γ (10 Units/ml). PGE2levels (measured by RIA) were determined in monocyte culture supernatants exposed during the following incubation periods: 0‐8, 8‐24, 24‐48, and 48‐72 h. Monocytes treated withSalmonellaLPS released 2 to 3‐fold greater amounts of PGE2than cells treated withBacteroidesspecies LPS preparations. Although IFN‐y alone did not stimulate PGE2 release,Bacteroides‐elicited PGE2release was siginificantly increased when monocytes were cultured concomitantly with IFN‐γ. PGE2release elicited bySalmonellaLPS was not significantly affected by interferon. These findings indicate that IFN‐γ can markedly potentiate the release of PGE2from monocytes stimulated withBacteroidesLPS. Furthermore, the observed weakness of these LPS preparations relative toSalmonellaLPS can be largely overcome by co‐treating monocytes with IFN‐γ.