Induction of prostaglandin release from macrophages by bacterial endotoxin.
This review summarizes the role of the monocytic responses to lipopolysaccharide as it relates to periodontal disease severity. Data are presented which illustrate that the levels of prostaglandin E2 (PGE2) secreted by systemic peripheral blood monocytes in culture, in the presence of bacterial endotoxins, are highly correlated with the levels observed in the gingival crevicular fluid. Furthermore, the different periodontal diagnostic categories have varying levels of monocytic and crevicular fluid PGE2, in juxtaposition with clinical disease severity. These data are consistent with the concept that there is close synchrony between the systemic responsiveness of peripheral blood monocytes with regard to prostanoid synthesis and the local levels of mediator present within the gingival crevice.
Offenbacher
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University of North Carolina at Chapel Hill, School of Dentistry, Department of Periodontology, Dental Research Center, 27599-7455, USA. steve_offenbacher@dentistry.unc.edu
Salvi
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D000328:Adult; D002478:Cells, Cultured; D003922:Diabetes Mellitus, Type 1 / Q000150:complications / Q000276:immunology / Q000503:physiopathology; D015232:Dinoprostone / Q000276:immunology / Q000378:metabolism*; D018450:Disease Progression; D004731:Endotoxins / Q000494:pharmacology*; D004926:Escherichia coli / Q000276:immunology; D005881:Gingiva / Q000378:metabolism; D006801:Humans; D018950:Lipopolysaccharide Receptors / Q000502:physiology; D008070:Lipopolysaccharides / Q000494:pharmacology*; D009000:Monocytes / Q000276:immunology / Q000378:metabolism*; D010518:Periodontitis / Q000276:immunology / Q000382:microbiology / Q000503:physiopathology*; D016966:Porphyromonas gingivalis / Q000276:immunology
D004731:Endotoxins; D018950:Lipopolysaccharide Receptors; D008070:Lipopolysaccharides; D015232:Dinoprostone