title: Serum modulation of neutrophil response to Porphyromonas gingivalis LPS in periodontal disease.
abstract: Rapidly progressive periodontitis is a form of early onset periodontitis characterised by severe gingival inflammation and rapid bone loss. Release of lipopolysaccharide (LPS) from the outer membrane of Gram negative bacteria initiates various biological activities including complement activation, cytotoxicity, and bone resorption. Serum from rapidly progressive periodontitis patients has been reported to enhance the superoxide response of normal neutrophils to lipopolysaccharide purified from Porphyromonas gingivalis, compared to control serum. The purpose of this study was to identify the factor in rapidly progressive periodontitis serum which is responsible for the enhancement of lipopolysaccharide activity. Candidate molecules were considered to be lipopolysaccharide binding protein or antibody to lipopolysaccharide. Lipopolysaccharide binding protein was quantified in serum by ELISA, and rapidly progressive periodontitis sera were found to contain two to three fold more lipopolysaccharide binding protein than control sera. Removal of lipopolysaccharide binding protein from either serum by adsorption to an anti lipopolysaccharide binding protein-sepharose affinity column removed the priming activity of normal neutrophils. Addition of exogenous lipopolysaccharide binding protein to control sera enhanced the priming activity in a dose dependent manner. These results suggest that lipopolysaccharide binding protein in rapidly progressive periodontitis serum may be responsible for enhancement of superoxide generation, which may result in more severe tissue damage in these patients.
authors.affiliation: Department of Periodontology, Eastman Dental Center, Rochester, New York, USA.
authors.forename: A S
authors.initials: AS
authors.lastname: Soolari
authors.forename: C
authors.initials: C
authors.lastname: Champagne
authors.forename: J S
authors.initials: JS
authors.lastname: Punzi
authors.forename: S
authors.initials: S
authors.lastname: Amar
authors.forename: T E
authors.initials: TE
authors.lastname: Van Dyke
mesh_terms: D000209:Acute-Phase Proteins / Q000032:analysis*; D000328:Adult; D016301:Alveolar Bone Loss / Q000382:microbiology; D000704:Analysis of Variance; D000907:Antibodies, Bacterial / Q000097:blood; D016866:Bacteroidaceae Infections / Q000097:blood*; D002352:Carrier Proteins / Q000032:analysis / Q000097:blood*; D002846:Chromatography, Affinity; D002847:Chromatography, Agarose; D004591:Electrophoresis, Polyacrylamide Gel; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D005891:Gingivitis / Q000382:microbiology; D006801:Humans; D007074:Immunoglobulin G / Q000097:blood; D008070:Lipopolysaccharides / Q000032:analysis / Q000097:blood*; D008297:Male; D008562:Membrane Glycoproteins; D018375:Neutrophil Activation / Q000502:physiology*; D009504:Neutrophils / Q000378:metabolism* / Q000382:microbiology; D016877:Oxidants / Q000378:metabolism; D010518:Periodontitis / Q000097:blood / Q000382:microbiology*; D016966:Porphyromonas gingivalis / Q000378:metabolism*; D013481:Superoxides / Q000378:metabolism; D000099231:Lipopolysaccharide-Binding Protein
chemical_list: D000209:Acute-Phase Proteins; D000907:Antibodies, Bacterial; D002352:Carrier Proteins; D007074:Immunoglobulin G; D008070:Lipopolysaccharides; D008562:Membrane Glycoproteins; D016877:Oxidants; D013481:Superoxides; D000099231:Lipopolysaccharide-Binding Protein