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Effects of CD14 receptors on tissue reactions induced by local injection of two gram‐negative bacterial lipopolysaccharides
Author(s) -
Chiang ChengYang,
Fu Earl,
Shen EChin,
Chiu HsienChung
Publication year - 2003
Publication title -
journal of periodontal research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.31
H-Index - 83
eISSN - 1600-0765
pISSN - 0022-3484
DOI - 10.1034/j.1600-0765.2003.01617.x
Subject(s) - bone resorption , cd14 , lipopolysaccharide , calvaria , inflammation , resorption , porphyromonas gingivalis , osteoclast , medicine , chemistry , endocrinology , periodontitis , receptor , biology , biochemistry , in vitro
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 µg 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 µg 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.