| Project/Area Number |
07044237
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| Research Category |
Grant-in-Aid for international Scientific Research
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| Allocation Type | Single-year Grants |
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| Section | Joint Research |
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| Research Institution | Niigata University |
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Principal Investigator |
HARA Koji Niigata University, School of Dentistry professor, 歯学部, 教授 (20018419)
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| Co-Investigator(Kenkyū-buntansha) |
JEANNEL Dominique Epidemiology of Oncogene Viruses Unit, Pasteur Institute Associate Professor, 助教授
TAI Hideaki Niigata University, School of Dentistry Dental Hospital Research Assistant, 歯学部附属病院, 助手 (30272826)
SUZUKI Takashi Niigata University, School of Dentistry Research Assistant, 歯学部, 助手 (00251827)
YOSHIE Hiromasa Niigata University, School of Dentistry Associate Professor, 歯学部, 助教授 (20143787)
GUY De the Epidemiology of Oncogene Viruses Unit, Pasteur Institute professor, 教授
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| Project Period (FY) |
1995
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| Project Status |
Completed (Fiscal Year 1995)
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| Budget Amount *help |
¥9,400,000 (Direct Cost: ¥9,400,000)
Fiscal Year 1995: ¥9,400,000 (Direct Cost: ¥9,400,000)
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| Keywords | HIV pathology / Periodontal lesion / Local immune response / Gingival crevicular fluid / Macrophages / Flow cytometry / Principal component analysis / Diagnostic criteria |
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| Research Abstract |
Objectives : To characterize the local immune response in AIDS-associated periodontal lesions and to assess the relationship between clinical and immunobiological parameters to propose diagnostic criteria of HIV-related periodontitis (HIV-P).
Methods : P24+ cell from Gingival crevicular fluid (GCF) leukocytes of CDC stage IV AIDS patients were characterized by flow cytometry (FCM). Peripheral blood (PB) leukocytes served as systemic controls. Numerical datasets were subjected to a principal component analysis (PCA).
Results : Of the 91 patients screened, 44 had HIV-P (48.35%). Two-color FCM of GCF cells from 15 patients disclosed a high p24+ macrophage fraction and a low CD16+CD11b+ neutrophil rate in GCF.Three-color FCM of 23 patients showed that CD68+/p24+ and CD14+/CD68+/p24+ fractions were significantly higher in GCF than in PB.CD14+/p24+ fraction is lower in GCF than in PB.The fluorescence intensities (F1) for p24 in CD14+ and CD14+/CD68+ cells were higher in GCF.The p24 FI of CD68+ macrophages in GCF inversely correlated with CD4+ lymphocytes count in PB.P24 FI levels of CD14+ monocytes in GCF and PB significantly correlated. PCA revealed 3 factors explaining over 75% of the variance : Factor 1 regulated by GI, LA and BL and % CD68/p24 ; Factor 2, regulated by % CD68/p24, BL and T4, where % CD68/p24 negatively correlated with the two other parameters ; Factor 3 was dominated by age, T4, BL.
Conclusion : Putatively HIV-infected p24+/CD68+ macrophages were detected from GCF.Downregulated CD16 on GCF neutrophil implied their de-activation. P24+ monocytes appeared mobilised from blood to the HIV-P lesions, then differentiate in situ into macrophages. HIV-P can be characterized by an aggressive tissue destruction and an infiltration of p24+ macrophages. PCA suggested that BL and p24+ macrophage mobilization may asynchronously occur over the disease course.
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