website: 86th General Session & Exhibition of the IADR

ABSTRACT: 2656  

Interaction of periodontopathogens with the phagocyte antioxidant/prooxydant system

C. BOUCHER, Universite Laval, Quebec, Canada, D. GRENIER, Universite Laval, Quebec City, Canada, and F. CHANDAD, Universite Laval, Quebec city, Canada

Phagocytes represent a powerful defense system against invading microorganisms. Stimulation of phagocytes with bacteria or their components activates various cell processes and modulates the cell redox status. Objective: The aim of this study was to investigate the effect of LPS of major periodontopathogens on activities and production of granulocyte antioxidant and prooxidant enzymes. Methods: Human neutrophil-like DMSO-differentiated HL-60 cells were stimulated with periodontopathogen LPS. The specific activities of catalase, manganese-superoxide dismutase (Mn-SOD) and glutathione S-transferase (GST) were quantified using enzymatic assays while protein production in cell lysates was detected by immunoblotting. NADPH subunits p22-phox and p47-phox, xanthine oxidase (XO) and myeloperoxidase (MPO) protein production was also analyzed by immunoblotting. Results: LPS of periodontopathogens induce a decrease in catalase activity and protein production and an increase in Mn-SOD activity and protein production. No significant differences were observed in GST activity. However, a GST protein overproduction was observed in LPS-stimulated cells. LPS of periodontopathogens increase the translocation of the cytosolic NADPH subunit p47-phox to the plasmic membrane. Differential production of XO was observed depending of the LPS used for cell stimulation. LPS of Fusobacterium nucelatum and Porphyromonas gingivalis increase the production of XO, while that of Aggregatibacter actinomycetemcomitans has no effect. Conclusion: These findings suggest that the modification of the redox status in neutrophils may contribute to the exacerbation of the effect of oxidative stress induced by periodontopathogens and may contribute to tissue destruction in periodontal diseases. This study was supported by Fonds Emile Beaulieu and Fondation de l'Ordre des dentistes du Québec.

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