Lindemann R A, Economou J S, Rothermel H
Section of Oral Diagnosis, Oral Medicine, and Oral Pathology, UCLA School of Dentistry.
J Dent Res. 1988 Aug;67(8):1131-5. doi: 10.1177/00220345880670081401.
Whole Gram-negative bacteria associated with juvenile and adult periodontitis, and their respective extracted lipopolysaccharides (LPS), were tested for the ability to activate quiescent human peripheral blood monocytes. All pathogenic Gram-negative bacteria and all LPS tested were able to induce the production of significant amounts of IL-1 and TNF, monokines known to induce osteoclastic bone resorption. Haemophilus segnis, which has not been associated with any form of periodontal disease, did not activate monocytes. Purified LPS from Actinobacillus actinomycetemcomitans Y4 was able to elicit IL-1 and TNF release at a threshold concentration of 1-10 ng/mL. To examine the mechanism whereby whole bacteria activated monocytes, we added polymixin B in culture with glutaraldehyde-fixed bacteria to bind LPS. This resulted in the abrogation of IL-1 and TNF production. To compare the effects of Gram-positive oral bacteria on monocytes, we also tested Staphylococcus epidermidis and the Gram-positive amphipathic equivalent of LPS, lipoteichoic acid (LTA) extracted from Staphylococcus aureus bacteria. Whereas whole Gram-positive bacteria had no stimulatory effect on monocytes, LTA induced IL-1 and TNF production at a concentration range equivalent to that of the LPS. These results indicate that monocytes are activated by free LPS or LPS bound to Gram-negative pathogenic periodontal bacteria to produce monokines which may contribute to the destruction of periodontal bone.
对与青少年和成人牙周炎相关的全革兰氏阴性菌及其各自提取的脂多糖(LPS)进行了测试,以检测其激活静息人类外周血单核细胞的能力。所有测试的致病性革兰氏阴性菌和所有LPS均能够诱导产生大量白细胞介素-1(IL-1)和肿瘤坏死因子(TNF),这两种单核因子已知可诱导破骨细胞性骨吸收。与任何形式的牙周疾病均无关联的迟缓嗜血杆菌未激活单核细胞。从伴放线放线杆菌Y4中纯化的LPS能够在1-10 ng/mL的阈值浓度下引发IL-1和TNF的释放。为了研究全细菌激活单核细胞的机制,我们在含有戊二醛固定细菌的培养物中加入多粘菌素B以结合LPS。这导致IL-1和TNF产生被消除。为了比较革兰氏阳性口腔细菌对单核细胞的影响,我们还测试了表皮葡萄球菌以及从金黄色葡萄球菌中提取的革兰氏阳性两亲性LPS等效物脂磷壁酸(LTA)。尽管全革兰氏阳性菌对单核细胞没有刺激作用,但LTA在与LPS相当的浓度范围内诱导了IL-1和TNF的产生。这些结果表明,单核细胞被游离的LPS或与革兰氏阴性致病性牙周细菌结合的LPS激活,从而产生可能导致牙周骨破坏的单核因子。