| Project/Area Number |
07457149
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Respiratory organ internal medicine
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| Research Institution | Kyorin University School of Medicine |
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Principal Investigator |
KOBAYASHI Hiroyuki Kyorin Univ.1st Dept.of Int.Med., Professor, 医学部, 教授 (40086509)
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| Co-Investigator(Kenkyū-buntansha) |
WATANABE Hidehiro Kyorin Univ.1st Dept.of Int.Med., Asistant, 医学部, 助手
KAWAI Shin Kyorin Univ.1st Dept.of Int.Med., Lecturer, 医学部, 講師 (70204667)
大垣 憲隆 杏林大学, 医学部, 助手
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| Project Period (FY) |
1995 – 1996
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| Project Status |
Completed (Fiscal Year 1996)
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| Budget Amount *help |
¥5,300,000 (Direct Cost: ¥5,300,000)
Fiscal Year 1996: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 1995: ¥4,400,000 (Direct Cost: ¥4,400,000)
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| Keywords | Airway biofilm / Immune reaction / Alginate / Immune Complex / Pathogenesis / Anti-biofilm / 免疫複合体 / 生体細胞作用 |
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| Research Abstract |
1. Clinical Manifestation of Airway Biofilm Disease
1) Invasive progress on airway biofilm disease
The mechanisms of invasive type exacerbation of biofilm disease can be explained. The floating type of bacteria released from biofilm will attched to other part of airway tissue. They have no mucoid-alginate, so they directly attach to tissue. Such a direct binding is so stimulant for tissue cell that they was make a new infectious lesion on attached tissue. This type of infectious exacerbation can be repeated in airway biofilm disease.
2) Immunologic progress on airway biofilm disease
Alginate, main component of bacterial biofilm, acts as an antigen to produce anti-alginate antibody in the host. It also exhibits an antigen antibody reaction locally in the small airways following infection, with resultant infiltration of lymphocytes. Furthermor, continued or repeated infection promotes these changes, leading to a narrowed or deformed airway due to lymphocyte follicules or granuloma like infiltrations. Excess antigen following persistent colonization of biofilm bactera forms circulating ICs. When the ICs deposit on the airway tissue, the complement-activated neutrophils bind to the Fc portion of deposited ICs, consequently resulting in the appearance of PMNs influx and tissue destruction due to these PMNs.
2. Basic Mechanisms of Macrolide Effect on Airway Biofilm Disease
The 14 and 15 membered macrolide suppress the antigen antibody reaction induced by alginate at small airway area and they inhibit the alginate production from bacteria due to the inhibition of the enzymatic activity of GMD enzyme placed on late stage of alginate synthetic pathway in bacterium. Then, these macrolide effects may decrese the circulating immune complex in airway biofilm disease. Even more, structural specific of macrolide compounds for such anti-alginate action is discussed.
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