Effects of CD14 receptors on tissue reactions induced by local injection of two gram-negative bacterial lipopolysaccharides.
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.
Chiang
Cheng-Yang
CY
Department of Periodontology, School of Dentistry, Tri-Service General Hospital, National Defense Medical Center, Taipei, Taiwan, ROC. dentalab@tpts5.seed.net.tw
Fu
Earl
E
Shen
E-Chin
EC
Chiu
Hsien-Chung
HC
D000135:Acid Phosphatase / Q000032:analysis; D000704:Analysis of Variance; D000818:Animals; D015415:Biomarkers / Q000032:analysis; D001862:Bone Resorption / Q000276:immunology / Q000473:pathology; D002452:Cell Count; D004396:Coloring Agents; D004195:Disease Models, Animal; D007527:Isoenzymes / Q000032:analysis; D018950:Lipopolysaccharide Receptors / Q000276:immunology*; D008070:Lipopolysaccharides / Q000276:immunology*; D008264:Macrophages / Q000276:immunology / Q000473:pathology; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D008815:Mice, Inbred Strains; D018345:Mice, Knockout; D009336:Necrosis; D010010:Osteoclasts / Q000276:immunology / Q000473:pathology; D016966:Porphyromonas gingivalis / Q000276:immunology*; D012475:Salmonella / Q000276:immunology*; D012867:Skin / Q000276:immunology / Q000473:pathology; D012886:Skull / Q000276:immunology / Q000473:pathology; D000071681:Tartrate-Resistant Acid Phosphatase
D015415:Biomarkers; D004396:Coloring Agents; D007527:Isoenzymes; D018950:Lipopolysaccharide Receptors; D008070:Lipopolysaccharides; D000135:Acid Phosphatase; C000605511:Acp5 protein, mouse; D000071681:Tartrate-Resistant Acid Phosphatase