1998 Fiscal Year Final Research Report Summary
Opsonophagocytic effect of antibody against recombinant 40-kDa OMP of P.gingivalis on neutrophils and induction of Th1 immune responses
| Project/Area Number |
09671935
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
病態科学系歯学(含放射線系歯学)
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| Research Institution | Nihon University |
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Principal Investigator |
SAITO Shigeno Nihon University School of Dentistry at Matsudo Biochemistry Instructor, 松戸歯学部, 講師 (60072394)
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| Project Period (FY) |
1997 – 1998
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| Keywords | Neutrophil / phagocytosis / Porphyromonas gingivalis / opsonization / Th1 immune responses |
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| Research Abstract |
Porphyromonas gingivalis is associated with the initiation and progression of adult periodontitis. The outer membrane proteins of the bacteria are potentially important targets for interaction with host defense systems. A 40-kDa OMP is conserved among many strains of P.gingivalis. For the development of recombinant 40-kDa OMP as a vaccine for passive immunization, the elucidation of the roles of the anti-r40-kDa OMP antibody in the host defense against P.gingivalis is essential. We demonstrated that r40-kDa OMP antibody in the presence of human complement successfully opsonized [^3H]-thymidine-labelled P.gingivalis as a target for phagocytosis by HL-60 cells differentiated with DMSO.The phagocytized bacteria were then intracellularly killed and lysed, and the radioactive degradation debris egested into the culture medium. We conclude that an antibody against r40-kDa OMP has an opsonic activity on human neutrophil function for phagocytosis of P.gingivalis. We might speculate that Th2 cells can be protective via the provision of help for antibody synthesis and that Th1 and CD8^+ T lymphocytes might be destructive via the prominent production of IFN-gamma and the potential stimulation of macrophage secretion of IL-1 and subsequent bone-destructive activity. Thus, T-cell features such as help[for antibody are important modulators of periodontal inflammation and therefore may be considered targets for disease intervention.
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