Hyporesponsiveness of inflamed human gingival fibroblasts from patients with chronic periodontal diseases against cell surface components of Porphyromonas gingivalis.

Hyporesponsiveness of inflamed human gingival fibroblasts from patients with chronic periodontal diseases against cell surface components of Porphyromonas gingivalis.
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慢性牙周病患者发炎的人牙龈成纤维细胞对牙龈卟啉单胞菌细胞表面成分的反应性低下。

DOI:
10.1111/j.1574-695x.1997.tb01023.x
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发表时间:
1997
影响因子:
--
通讯作者:
H. Uchida
H. Uchida
中科院分区:
--
文献类型:
--
作者:
T. Ogawa;Akiko Ozaki;H. Shimauchi;H. Uchida

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Inflamed human gingival fibroblasts (HGF) of patients with chronic periodontal diseases have less active interleukin-8 (IL-8) production compared with normal HGF of volunteers with healthy gingival tissues, after stimulation with Porphyromonas gingivalis surface components such as fimbriae, lipopolysaccharide (LPS) and its lipid A, but not LPS or lipid A from other bacterial species. A decrease in number of specific binding sites for P. gingivalis fimbrial molecules in inflamed HGF is also observed by Scatchard plot analysis. A short exposure (6 h) to P. gingivalis LPS resulted in significant potentiation of the LPS-dependent IL-8 production in normal HGF, whereas a long exposure (48 h) to the LPS significantly reduced IL-8 production. Tyrosine phosphorylation of proteins of 127 kDa and 186 kDa in inflamed HGF stimulated with P. gingivalis fimbriae or its LPS was observed by immunoblotting, and these two phosphoproteins were termed tolerance-induced protein, TIP. Protein bands of 45 kDa which bound to radioiodinated P. gingivalis fimbriae in the presence and absence of fetal bovine serum (FBS), and major 73-kDa and minor 30-kDa and 45-kDa bands which bound to radioiodinated P. gingivalis LPS in the presence of FBS in normal and inflamed HGF were observed by using photocrosslinking. These findings suggest that the hyporesponsiveness of HGF induced by a prolonged exposure to P. gingivalis may emerge because of HGF damage or result from host defense in chronic periodontal lesions.
通过光亲和交联鉴定 70Z/3 细胞中的脂多糖结合蛋白。
DOI: --
发表时间: 1990
期刊: The Journal of biological chemistry
影响因子: --
作者:
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人巨噬细胞中脂多糖诱导的蛋白酪氨酸磷酸化是由 CD14 介导的。
DOI: --
发表时间: 1993
期刊: Journal of immunology (Baltimore, Md. : 1950)
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DOI: --
发表时间: 1988
期刊: Journal of immunology (Baltimore, Md. : 1950)
影响因子: --
作者:
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脂多糖 (LPS) 与淋巴网状细胞上的 73-kDa 和 38-kDa 表面蛋白结合:球形红假单胞菌脂质 A 优先抑制 LPS 与前者的结合。
DOI: 10.1016/0165-2478(93)90096-k
发表时间: 1993
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影响因子: 4.4
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Lei,MG;Qureshi,N;Morrison,DC
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