Experimental pathological study on roles of chemokines in LPS-induced periodontal tissue destruction - Basic analysis on remedical effects of specific antibody against chemokine -

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1. Immunoexpression of macrophage inflammatory protein-2 (MIP-2) and macrophage chemoattractant protein-1 (MCP-l) in rat periodontal tissue after topical application of Lipopolysaccharide (LPS) : 1) Topically applied 5 mg/ml E. Coli LPS from rat gingival sulcus rapidly provoked inflammatory changes in junctional epithelium (JE) and sub-JE area. In addition, stimulation of osteoclastic bone resorption along the alveolar bone surface showing a biphasic response peaking at 3 hours and 3 days was observed. 2) A transient immuno-expression of MIP-2 in JE cells peaking at 1 day was observed. Corresponding to excessive MIP-2 expression, LPS application induced a significant increase in number of neutrophils in JE and sub-JE area. 3) At day 1 and 2 after LPS application, immunoexpression of MCP-1 in osteoblasts and osteocytes presented in alveolar crestal area was observed. The MCP-1 production from these cells may cause local recruitment of preosteoclasts and the following osteoclastic bone r … More esorption at day 3.2. Application of various concentrations of MIP-2 : Various concentrations of recombinant rat MIP-2 (0.05, 0.5, 5, 50 μg/ml) applied from gingival sulcus caused not only neutrophil recruitment into JE and sub-JE area but also osteoclasts amassment along the alveolar bone surface in a dose dependent manner3. Effects of previously intraperitoneal-injected anti-MIP-2 antibody on periodontal tissue destruction caused by LPS-application : Injection of the anti-MIP-2 antibody remarkably reduced the recruitment of neutrophils into JE and sub-JE area and significantly decreased the appearance of osteoclasts at 3 days after LPS application. On the other hand, the first increase of osteoclasts at 3 hours, which is seemed to be a direct effect of LPS, was not inhibited by the anti-MIP-2 antibody treatment. Theses findings indicated that MIP-2 may be one of powerful CXC-chemokines for neutrophil recruitment into the periodontal disease site and may play an important role in the initiation of inflammation. Moreover, the over secretion of CXC-chemokine in the periodontal disease site may induce production of various osteoclast stimulating factors resulting in the subsequent alveolar bone destruction. It is suggested a possibility of establishment new periodontal therapy targeting CXC-chemokine. Less