牙周病细菌免疫生物学活性的研究。牙龈拟杆菌与黏性放线菌可溶性组分活性比较。

K Matsubara
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引用次数: 0

摘要

牙龈拟杆菌和粘放线菌是牙周炎和牙龈炎的重要致病因子。本实验研究了牙龈白僵菌和粘胶白僵菌声波提取物对小鼠淋巴细胞DNA合成、人外周血单核细胞前列腺素E2 (PGE2)、胶原酶和白细胞介素1 (IL-1)产生的影响。此外,用细菌超声提取物培养的巨噬细胞条件培养基(MCM)刺激人牙周韧带(HPLF)和牙龈(Gin 1)成纤维细胞,检测PGE2和胶原酶的产生。所得结果如下:1. 超声提取液(10微克/毫升蛋白)对脾细胞有丝分裂活性较低,但可诱导多克隆B细胞活化。2. 虽然未发现这些声波提取物对人外周血单核细胞产生PGE2和胶原酶的影响,但已确认其诱导IL-1的产生。3.用龈芽孢杆菌和粘芽孢杆菌超声提取物刺激C3H/HeN小鼠腹腔巨噬细胞培养上清液,用HPLF和Gin 1诱导PGE2和胶原酶的产生。提示牙龈芽孢杆菌和粘胶芽孢杆菌的细胞成分可能通过刺激巨噬细胞和/或淋巴细胞在牙周组织破坏中起致病性作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
[Studies on immunobiological activities of periodontopathic bacteria. Comparison of the activities of soluble components from Bacteroides gingivalis and Actinomyces viscosus].

It has been proposed that Bacteroides gingivalis and Actinomyces viscosus are most important agents to pathogenesis of the periodontitis and gingivitis. In this study, the influences of sonic extracts prepared from B. gingivalis and A. viscosus for DNA synthesis of murine lymphocytes, production of prostaglandin E2 (PGE2), collagenase and interleukin-1 (IL-1) from human peripheral monocyte were investigated. Furthermore, PGE2 and collagenase production by fibroblasts from human periodontal ligament (HPLF) and gingiva (Gin 1) stimulated with macrophage conditioned medium (MCM) cultured with bacterial sonic extracts were examined. The results obtained were as follows. 1. The sonic extracts (10 micrograms/ml protein) from B. gingivalis and A. viscosus showd low mitogenic activity to spleen cells, however, induced polyclonal B cell activation. 2. Although, the effect of these sonic extracts on the production of PGE2 and collagenase by human peripheral monocyte was not found, the induction of IL-1 production was recognized. 3. The culture supernatants of C3H/HeN mouse peritoneal macrophage stimulated with sonic extracts of B. gingivalis and A. viscosus were induced PGE2 and collagenase production by HPLF and Gin 1. These results suggest that the cellular components of B. gingivalis and A. viscosus may play the pathogenic roles in periodontal tissue destruction through the stimulation of macrophage and/or lymphocyte.

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