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首页> 外文期刊>Infection and immunity >Lipopolysaccharides (LPS) of Oral Black-Pigmented Bacteria Induce Tumor Necrosis Factor Production by LPS-Refractory C3H/HeJ Macrophages in a Way Different from That of Salmonella LPS
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Lipopolysaccharides (LPS) of Oral Black-Pigmented Bacteria Induce Tumor Necrosis Factor Production by LPS-Refractory C3H/HeJ Macrophages in a Way Different from That of Salmonella LPS

机译：口服黑色色素细菌的脂多糖（LPS）诱导LPS难治性C3H / HeJ巨噬细胞产生沙门氏菌LPS的方式产生肿瘤坏死因子

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Some lipopolysaccharide (LPS) preparations from S- or R-form members of the family Enterobacteriaceae and oral black-pigmented bacteria (Porphyromonas gingivalis andPrevotella intermedia) are known to activate LPS-refractory C3H/HeJ macrophages. When contaminating proteins are removed from R-form LPS ofEnterobacteriaceae by repurification, however, this ability is lost. In the present study, we investigated the capacity of LPS from P. gingivalis, P. intermedia,Salmonella minnesota, and Salmonella abortusequi to induce production of tumor necrosis factor (TNF) in gamma interferon-primed C3H/HeJ macrophages before and after repurification. P. abortusequi S-LPS was fractionated by centrifugal partition chromatography into two LPS forms: SL-LPS, having homologous long O-polysaccharide chains, and SS-LPS having short oligosaccharide chains. Prior to repurification, all LPS forms except SL-LPS induced TNF production in both C3H/HeJ and C3H/HeN macrophages. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis showed that repurification removed contaminating protein from the preparations, and repurified SS-LPS and S. minnesota Ra-LPS no longer stimulated TNF production in C3H/HeJ macrophages, although C3H/HeN macrophages remained responsive. In contrast, repurified oral bacterial LPS retained the capacity to induce TNF production in C3H/HeJ macrophages. Oral bacterial LPS preparations also were not antagonized by excess inactive, repurified SL-LPS; Ra-LPS; Rhodobacter sphaeroides lipid A, a competitive LPS antagonist, or paclitaxel, an LPS agonist, and they were comparatively resistant to polymyxin B treatment. Nevertheless, oral bacterial LPS was less toxic tod-galactosamine-treated C3H/HeN mice than was LPS fromSalmonella. These findings indicate that the active molecule(s) and mode of action of LPS from P. gingivalisand P. intermedia are quite different from those of LPS from Salmonella.
机译：来自肠杆菌科和口腔黑色色素细菌（牙龈卟啉单胞菌和中间肠杆菌）的S型或R型成员的一些脂多糖（LPS）制剂>）可以激活LPS难治性C3H / HeJ巨噬细胞。但是，当通过重新纯化从肠杆菌科的R型LPS中除去污染蛋白时，这种能力就会丧失。在本研究中，我们调查了 P的LPS的容量。牙龈炎， P。培养基，沙门氏菌和 salmonella abortusequi 在再纯化前后诱导γ干扰素引发的C3H / HeJ巨噬细胞中诱导肿瘤坏死因子（TNF）的产生。 P。通过离心分配色谱法将abortusequi S-LPS分为两种LPS形式：具有同源的长O-多糖链的SL-LPS和具有短的寡糖链的SS-LPS。再纯化之前，除了SL-LPS以外，所有LPS形式均会在C3H / HeJ和C3H / HeN巨噬细胞中诱导TNF的产生。十二烷基硫酸钠-聚丙烯酰胺凝胶电泳表明，重新纯化去除了制备物中的污染蛋白，并再次纯化了SS-LPS和 S。尽管C3H / HeN巨噬细胞仍然具有反应性，但明尼苏达州的Ra-LPS不再刺激C3H / HeJ巨噬细胞中TNF的产生。相反，再纯化的口腔细菌LPS保留了在C3H / HeJ巨噬细胞中诱导TNF产生的能力。口服细菌LPS制剂也没有被过量的非活性，纯化的SL-LPS所拮抗。 Ra-LPS;竞争性LPS拮抗剂 sphaeroides sphaeroides 脂质A或LPS激动剂紫杉醇，它们对多粘菌素B的治疗具有相对的抗性。尽管如此，口服细菌LPS对Tod-半乳糖胺处理的C3H / HeN小鼠的毒性要小于沙门氏菌的LPS。这些发现表明来自 P的LPS的活性分子和作用方式。牙龈炎和 P。 intermedia 与沙门氏菌的LPS完全不同。

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