Journal
JOURNAL OF ENDODONTICS
Volume 33, Issue 11, Pages 1309-1312Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.joen.2007.08.001
Keywords
cyclooxygenase-2; inflammation; interleukin-1 beta; osteoblast; tumor necrosis factor-alpha
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Many of the proinflammatory effects of interleukin (IL)-1 beta and tumor necrosis factor-alpha (TNF-alpha) are mediated through cyclooxygenase-2 (COX-2)-dependent prostaglandin E2 (PGE2). The purpose of this study was to examine the expression of IL-1 beta and TNF-alpha in COX-2-deficient osteoblasts during inflammation. Primary osteoblasts prepared from wild-type (WT) and COX-2 knockout (K/O) mice were exposed to lipopolysaccharide (LPS) and endodontic obturation materials. An enzyme-linked immunosorbent assay was used to measure cytokine levels. LPS treatment led to a significant upregulation in IL-1 beta and TNF-alpha levels in both WT and K/0 cells. TNF-a upregulation in response to LPS was much more pronounced in K/0 cells compared with WT cells (p < 0.05). All materials tested except for gutta percha caused an increase in IL-1 beta expression. In conclusion, there appears to be a positive feedback regulation between TNF-a and COX-2-dependent PGE2 during LPS-induced inflammatory reactions.
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