1990 Fiscal Year Final Research Report Summary
The Research on the Pathogenesis of Branhamella Catarrhalis Respiratory Infections.
| Project/Area Number |
63480211
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Respiratory organ internal medicine
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| Research Institution | Nagasaki University |
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Principal Investigator |
NATSUMOTO Keizo Nagasaki University Institute of Tropical Medicine Professor, 熱帯医学研究所, 教授 (40004767)
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| Co-Investigator(Kenkyū-buntansha) |
TAKASUGI Masakazu Nagasaki University Hospital of Medicine Research Associate, 医学部・附属病院, 助手 (90163203)
TAKAHASHI Astushi Nagasaki University Hospital of Medicine Research Associate, 医学部・附属病院, 助手 (50171468)
OISHI Kazunori Nagasaki University Institute of Tropical Medicine Research Associate, 熱帯医学研究所, 助手 (80160414)
RIKITOMI Naoto Nagasaki University Hospital of Medicine Assistant Professor, 医学部・附属病院, 講師 (70175032)
NAGATAKE Tsuyoshi Nagasaki University Institute of Tropical Medicine Associate Professor, 熱帯医学研究所, 助教授 (30164445)
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| Project Period (FY) |
1988 – 1990
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| Keywords | Branhamella catarrhalis / Respiratory infections. / Lipopolysaccharide / Bacterial attachment / Monoclinal antibody |
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| Research Abstract |
A electromicroscopic study demonstrated the presence of fimbriae in 80% of freshly isolated Branhamella catarrhalis (B. C) strains. We also documented that the fimbriae of B. C mediated the attachment of B. C to human buccal epithelial cells using anti-fimbriae rabbit serum. Additionally, we confirmed that B. C attach to human tracheal cells several times higher than to human buccal epithelial cells. We also demonstrated the presence of the capsule of B. C by electromicroscopic observation.
We purified and characterized lipopolysaccharide (LPS) from B. C, and demonstrated that LPS was lipooligosaccharide (LOS), lacking of O-side chain, and that SDS-PAGE patterns of LPSs were different each other. We found a significant elevation of IgG antibody to B. C LOS in convalescent serum from patients with B. C respiratory infection. To investigate the role of anti-B. C LOS antibody, we evaluated 1) antibody-dependent, complement-mediated killing of B. C employing fresh convalescent serum from patients, and 2) protective effect of a murine monoclonal antibody (mAb) in a exprimental B. C pneumonia in mice. From these studies, it was concluded that anti-LOS antibody in patient serum caused complement-dependent killing against serum resistant B. C, and anti-LOS antibody provided a protective activity in vivo.
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