Contribution of interleukin-11 and prostaglandin(s) in lipopolysaccharide-induced bone resorption in vivo
OA Version
Citation
Abstract
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]
Description
Thesis (M.S.D.)--Boston University, Henry M. Goldman School of Dental Medicine, 2002 (Periodontology and Oral Biology).
Includes bibliographical references (leaves 58-73).
Includes bibliographical references (leaves 58-73).
License
This work is being made available in OpenBU by permission of its author, and is available for research purposes only. All rights are reserved to the author.