Production of interleukin-1 and tumor necrosis factor by human peripheral monocytes activated by periodontal bacteria and extracted lipopolysaccharides

Whole Gram-negative bacteria associated with juvenile and adult periodontitis, and their respective extracted lipopolysaccharides (LPS), were tested for the ability to activate quiescent human peripheral blood monocytes. All pathogenic Gram-negative bacteria and all LPS tested were able to induce th...

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Published in:Journal of dental research Vol. 67; no. 8; p. 1131
Main Authors: Lindemann, R A, Economou, J S, Rothermel, H
Format: Journal Article
Language:English
Published: United States 01.08.1988
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ISSN:0022-0345
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Summary:Whole Gram-negative bacteria associated with juvenile and adult periodontitis, and their respective extracted lipopolysaccharides (LPS), were tested for the ability to activate quiescent human peripheral blood monocytes. All pathogenic Gram-negative bacteria and all LPS tested were able to induce the production of significant amounts of IL-1 and TNF, monokines known to induce osteoclastic bone resorption. Haemophilus segnis, which has not been associated with any form of periodontal disease, did not activate monocytes. Purified LPS from Actinobacillus actinomycetemcomitans Y4 was able to elicit IL-1 and TNF release at a threshold concentration of 1-10 ng/mL. To examine the mechanism whereby whole bacteria activated monocytes, we added polymixin B in culture with glutaraldehyde-fixed bacteria to bind LPS. This resulted in the abrogation of IL-1 and TNF production. To compare the effects of Gram-positive oral bacteria on monocytes, we also tested Staphylococcus epidermidis and the Gram-positive amphipathic equivalent of LPS, lipoteichoic acid (LTA) extracted from Staphylococcus aureus bacteria. Whereas whole Gram-positive bacteria had no stimulatory effect on monocytes, LTA induced IL-1 and TNF production at a concentration range equivalent to that of the LPS. These results indicate that monocytes are activated by free LPS or LPS bound to Gram-negative pathogenic periodontal bacteria to produce monokines which may contribute to the destruction of periodontal bone.
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ISSN:0022-0345
DOI:10.1177/00220345880670081401