Priming effect of Porphyromonas gingivalis lipopolysaccharide on superoxide production by neutrophils from healthy and rapidly progressive periodontitis subjects.

Pre-incubation of neutrophils from rapidly progressive periodontitis (RPP) patients with lipopolysaccharide (LPS) extracted from Porphyromonas gingivalis was found to prime the neutrophils for enhanced FMLP-stimulated superoxide production in a dose-dependent manner. The priming effect of P. gingivalis LPS on neutrophils from control subjects was scanty or without effect at all. Inclusion of human serum in the experimental priming conditions increased the control and RPP neutrophil response by 2 to 3 fold. Blocking of the CD14 receptor on the neutrophil surface with monoclonal antibody eliminated the priming effect. Furthermore, incubation of control neutrophils with P. gingivalis LPS in the presence of serum from RPP patients generated a higher response as compared to incubation with control serum. The data suggest that neutrophil priming described in RPP patients is dependent on a serum factor which alters the neutrophil response to priming agents such as LPS.

[1]  L. Shapira,et al.  The Role of the Host Response in Periodontal Disease Progression: Implications for Future Treatment Strategies. , 1993, Journal of periodontology.

[2]  K. Kato,et al.  Cross-linking of lipopolysaccharide (LPS) to CD14 on THP-1 cells mediated by LPS-binding protein. , 1993, Journal of immunology.

[3]  S. Wright,et al.  Septin: a factor in plasma that opsonizes lipopolysaccharide-bearing particles for recognition by CD14 on phagocytes , 1992, The Journal of experimental medicine.

[4]  S. Socransky,et al.  The Bacterial Etiology of Destructive Periodontal Disease: Current Concepts. , 1992, Journal of periodontology.

[5]  R. Sha’afi,et al.  Lipopolysaccharide and serum cause the translocation of G-protein to the membrane and prime neutrophils via CD14. , 1992, Biochemical and biophysical research communications.

[6]  R. Page,et al.  Humoral immune responses to Porphyromonas gingivalis before and following therapy in rapidly progressive periodontitis patients. , 1991, Journal of periodontology.

[7]  J. Klein,et al.  Priming of the HL-60 cell respiratory burst response by tumor necrosis factor-alpha. , 1991, Lymphokine and cytokine research.

[8]  G. Whyte,et al.  Chemiluminescence of peripheral polymorphonuclear leukocytes from adult periodontitis patients. , 1989, Journal of clinical periodontology.

[9]  J. Sterne,et al.  Detection of high-risk groups and individuals for periodontal diseases. Evidence for the existence of high-risk groups and individuals and approaches to their detection. , 1988, Journal of clinical periodontology.

[10]  M. Vadas,et al.  Recombinant human tumor necrosis factor-alpha. Regulation of N-formylmethionylleucylphenylalanine receptor affinity and function on human neutrophils. , 1988, The Journal of clinical investigation.

[11]  B. Babior.  Oxidants from phagocytes: agents of defense and destruction. , 1984, Blood.

[12]  B. Åsman,et al.  Increased luminol enhanced chemiluminescence from peripheral granulocytes in juvenile periodontitis. , 1984, Scandinavian journal of dental research.

[13]  R. Johnston,et al.  Mechanisms of lipopolysaccharide priming for enhanced respiratory burst activity in human neutrophils. , 1991, Advances in experimental medicine and biology.

[14]  A. Ferrante,et al.  Effects of tumour necrosis factor alpha and interleukin-1 alpha and beta on human neutrophil migration, respiratory burst and degranulation. , 1988, International archives of allergy and applied immunology.

[15]  T. E. Winford,et al.  Neutrophil chemi-luminescence and opsonic activities of young people with periodontitis in Thailand. , 1984, Archives of oral biology.