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
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
复制标题
口腔黑色素细菌的脂多糖 (LPS) 以与沙门氏菌 LPS 不同的方式诱导 LPS 难治性 C3H/HeJ 巨噬细胞产生肿瘤坏死因子
作者:
T. Kirikae;T. Nitta;F. Kirikae;Y. Suda;S. Kusumoto;Nirofer Qureshi;M. Nakano
ABSTRACT 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.
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影响因子:
56.9
作者:
DING, AH;PORTEU, F;NATHAN, CF
通讯作者:
NATHAN, CF
影响因子:
4.4
作者:
C. Amura;L. C. Chen;N. Hirohashi;M. Lei;D. Morrison
通讯作者:
C. Amura;L. C. Chen;N. Hirohashi;M. Lei;D. Morrison
DOI:
--
发表时间:
1991
期刊:
The Journal of biological chemistry
影响因子:
--
作者:
Qureshi,N;Takayama,K;Meyer,KC;Kirkland,TN;Bush,CA;Chen,L;Wang,R;Cotter,RJ
通讯作者:
Cotter,RJ
影响因子:
--
作者:
Bramanti,TE;Wong,GG;Weintraub,ST;Holt,SC
通讯作者:
Holt,SC
DOI:
10.1016/s0021-9258(18)55023-7
发表时间:
1991-10
期刊:
The Journal of biological chemistry
影响因子:
--
作者:
Douglas T. GolenbockSQll;Randolph;HamptonIIQ;N. Qureshi;K. Takayama;Christian R. H. RaetzQ
通讯作者:
Douglas T. GolenbockSQll;Randolph;HamptonIIQ;N. Qureshi;K. Takayama;Christian R. H. RaetzQ