Contribution of interleukin-11 and prostaglandin(s) in lipopolysaccharide-induced bone resorption in vivo
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We previously demonstrated that interleukin- I (IL-1) and tumor necrosis factor (TNF) activities only partially account for calvarial bone resorption induced by local application of lipopolysaccharide (LPS) in mice. The present study was undertaken to determine the role and relative contribution of IL-11 and prostaglandin(s) (PGs) in LPS-induced bone resorption in vivo. One-time dose of LPS was injected into the subcutaneous tissue overlying the calvariae of IL-lRi- 1 - TNFRp5S-1--IL-1Rl _1 _ and wild-type mice. Mice were then treated with injections of anti-It -11 monoclonal antibody (mAb ), indomethacin or PBS and sacrificed 5 days later. Histological sections stained for TRAP were quantified by histomorphometric analysis. At low dose of LPS (100 μg/mouse), the percentage of bone surface covered by osteoclasts was found similar in three strains of mice. The increase was reduced by 50% with anti-IL-11 mAb and by 60% with indomethacin. At higher doses of LPS (500 μg/mouse), we found an 8-fold increase in wild type and 5-fold in IL-lRl _1 _ and TNFRp55-1--IL-1Rl _1 _ mice after normalizing with the value from saline+PBS control group in the same strain of mice. The increase was reduced by 63 and 78% in wildtype mice, and by about 73 and 84% in IL-lRi- 1 - and TNFRp5S-1--IL-1R1_1 _ mice treated with anti-IL-11 mAb or indomethacin respectively. Our findings suggest that in vivo at low-dose (100 μg/mouse), LPS-induced bone resorption is mediated ... [TRUNCATED]
Thesis (M.S.D.)--Boston University, Henry M. Goldman School of Dental Medicine, 2002 (Periodontology and Oral Biology).Includes bibliographical references (leaves 58-73).
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