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PMID: 10417196 Published · ppublish English Journal Article Research Support, U.S. Gov't, P.H.S.

Interleukin-1 and tumor necrosis factor activities partially account for calvarial bone resorption induced by local injection of lipopolysaccharide.

Infection and immunity ·Vol. 67 ·No. 8 ·1999-08-00 ·Pages 4231-6

Chiang CY, Kyritsis G, Graves DT, Amar S

Abstract

The present study was undertaken to test the hypothesis that tumor necrosis factor (TNF) and/or interleukin-1 (IL-1) activity mediates lipopolysaccharide (LPS)-induced bone resorption in vivo. To test this hypothesis, Escherichia coli LPS or Porphyromonas gingivalis LPS was injected into the subcutaneous tissues overlying mouse calvariae. Histological sections, prepared from the center of the lesion, were stained for tartrate-resistant acid phosphatase, and histomorphometric analysis was performed to quantify the osteoclast number and the area of bone resorption. In time course experiments using normal mice, a peak of bone resorption occurred 5 days after endotoxin stimulation. In dose-response experiments, IL-1 receptor type 1 deletion (IL-1R(-/-)), TNF double-receptor p55/p75 deletion (TNF p55(-/-)/p75(-/-)), combined TNF p55 and IL-1 receptor type 1 deletion (TNF p55(-/-)/IL-1R(-/-)), and IL-1beta-converting enzyme-deficient (ICE(-/-)) mice and the respective wild-type mice were injected with 500, 100, or 20 micrograms of P. gingivalis LPS and sacrificed 5 days after LPS injection. At the highest dose (500 micrograms), significant decreases in osteoclast number occurred in mutant mice compared to wild-type mice: (i) a 64% reduction for the TNF p55(-/-)/IL-1R(-/-) mice, (ii) a 57% reduction for the IL-1R(-/-) mice, (iii) a 41% reduction for the TNF p55(-/-)/p75(-/-) mice, and (iv) a 38% reduction for the ICE(-/-) mice. At the two lower doses, bone resorption was apparent but no significant differences between mutant and wild-type animals were observed. The present data indicate that at higher doses, LPS-induced bone resorption is substantially mediated by IL-1 and TNF receptor signaling. Furthermore, IL-1 receptor signaling appears to be slightly more important than TNF receptor signaling. At lower LPS doses, other pathways leading to osteoclast activity that are independent of TNF and IL-1 are involved.

MeSH Terms
Animals Bone Resorption/etiology Dose-Response Relationship, Drug Interleukin-1/physiology Lipopolysaccharides/toxicity Mice Mice, Inbred C57BL Mice, Transgenic Receptors, Interleukin-1/physiology Receptors, Tumor Necrosis Factor/physiology Skull Time Factors Tumor Necrosis Factor-alpha/physiology
Chemicals
Interleukin-1 Lipopolysaccharides Receptors, Interleukin-1 Receptors, Tumor Necrosis Factor Tumor Necrosis Factor-alpha
Authors & Affiliations
4 authors, click to expand affiliations / ORCID
Chiang C Y
Department of Periodontology and Oral Biology, School of Dental Medicine, Boston University, Boston, Massachusetts 02118, USA.
Kyritsis G
Graves D T
Amar S
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Article Info
Journal
Infection and immunity
Abbr.
Infect Immun
ISSN
0019-9567
DOI
10.1128/IAI.67.8.4231-4236.1999
Published
1999-08-00
Pages
4231-6
Language
English
Region
United States
NLM ID
0246127
PMCID
PMC96729
Subset
IM
Grants
NIDCR NIH HHS · R01 DE011254 · United States
NIDCR NIH HHS · DE10799 · United States
NIDCR NIH HHS · DE11254 · United States
External Links
PubMed source DOI: 10.1128/IAI.67.8.4231-4236.1999 PMC Full Text View journal details
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