Chiang Cheng-Yang, Fu Earl, Shen E-Chin, Chiu Hsien-Chung
Department of Periodontology, School of Dentistry, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan, ROC.
J Periodontal Res. 2003 Feb;38(1):36-43. doi: 10.1034/j.1600-0765.2003.01617.x.
Lipopolysaccharide (LPS) was recognized by CD14, which may be an important mediator in the deleterious effects of LPS on the periodontal destruction. To investigate the roles of CD14 molecules on LPS-induced soft tissue inflammation and bone destruction, the tissues of CD14-deficient mice were examined histopathologically following a local injection of either Salmonella minnesota or Porphyromonas gingivalis LPS. In the first group, 12 mice received a local injection of 500 microg of purified P. gingivalis LPS and six mice were injected with saline to the calvaria as controls. In the second group 13 mice were injected subcutaneously on the laterally abdominal skin with 50 microg of S. minnesota LPS and three mice were injected with PBS. Mice were sacrificed at day 5. After histological preparation, the tissue sections of calvaria and soft tissue specimen were stained with tartrate-resistant acid phosphatase (TRAP) marker for osteoclast and macrophage. The soft tissue sections were also stained with hematoxylin & eosin (H&E). Resorption surface and osteoclast index were measured to quantify bone resorption. Necrotic area and inflammatory cell numbers were estimated to assess the situation of local inflammation. Our results indicated that LPS-induced bone resorption is inhibited in CD14-deficient mice. An increase in the number of total inflammatory cells was noticed in both CD14-deficient mice and wild-type mice; however, the cell numbers were less in CD14-deficient mice than those in wild-type mice (two- to three-fold decrease). Therefore, we conclude that the LPS-stimulated bone resorption is mainly via CD14 receptor but the LPS-induced soft tissue inflammation appears to be partially dependent on the receptor.
脂多糖(LPS)可被CD14识别,CD14可能是LPS对牙周组织破坏产生有害作用的重要介质。为了研究CD14分子在LPS诱导的软组织炎症和骨破坏中的作用,在局部注射明尼苏达沙门氏菌或牙龈卟啉单胞菌LPS后,对CD14缺陷小鼠的组织进行了组织病理学检查。在第一组中,12只小鼠接受了500微克纯化牙龈卟啉单胞菌LPS的局部注射,6只小鼠接受颅骨生理盐水注射作为对照。在第二组中,13只小鼠在侧腹部皮肤皮下注射50微克明尼苏达沙门氏菌LPS,3只小鼠注射磷酸盐缓冲液(PBS)。在第5天处死小鼠。经过组织学处理后,颅骨组织切片和软组织标本用抗酒石酸酸性磷酸酶(TRAP)标记染色,以检测破骨细胞和巨噬细胞。软组织切片也用苏木精和伊红(H&E)染色。测量吸收表面和破骨细胞指数以量化骨吸收。估计坏死面积和炎性细胞数量以评估局部炎症情况。我们的结果表明,在CD14缺陷小鼠中,LPS诱导的骨吸收受到抑制。在CD14缺陷小鼠和野生型小鼠中均观察到总炎性细胞数量增加;然而,CD14缺陷小鼠中的细胞数量比野生型小鼠中的细胞数量少(减少两到三倍)。因此,我们得出结论,LPS刺激的骨吸收主要通过CD14受体,但LPS诱导的软组织炎症似乎部分依赖于该受体。