2001 Fiscal Year Final Research Report Summary
Antimicrobial activities of catechin, catechin-antibiotic combinations and mechanisms
| Project/Area Number |
11470071
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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 |
Bacteriology (including Mycology)
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| Research Institution | Showa University |
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Principal Investigator |
SHIMAMURA Tadakatsu Showa University, School of Medicine, Department of Microbiology and Immunology, Professor, 医学部, 教授 (50056149)
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| Co-Investigator(Kenkyū-buntansha) |
HU Zhi-Qing Showa University, School of Medicine, Department of Microbiology and Immunology, Associate Professor, 医学部, 助教授 (60245826)
OKUBO Sachie Showa University, School of Medicine, Department of Microbiology and Immunology, Assistant Professor, 医学部, 講師 (40053938)
ZHAO Wei-Hua Showa University, School of Medicine, Department of Microbiology and Immunology, Assistant, 医学部, 助手 (90327916)
YANAGAWA Yoko Showa University, School of Medicine, Department of Microbiology and Immunology, Assistant, 医学部, 助手 (20307044)
YAMAGUCHI Koushi Showa University, School of Medicine, Department of Microbiology and Immunology, Assistant Professor (70210359)
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| Project Period (FY) |
1999 – 2001
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| Keywords | Catechin / Antimicrobial / Antibiotics / Combination effect / MRSA / Helicobacter pylori / HIV / Salmonella |
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| Research Abstract |
The antimicrobial activities of catechin, catechin-antibiotic combinations and mechanism were investigated in this project.
Firstly, the potent synergy was obtained in combinations of EGCg, the main component of tea catechins, with β-lactams against MRSA, especially in the combination with carbapenems. The interference with the integrity and biosynthesis of cell wall is responsible for the synergism, owing to the direct binding of EGCg with peptidoglycan. The combinations of EGCg with the inhibitors of either protein or nuclear acid synthesis showed additive or indifferent effects. An antagonistic tendency against glycopeptide antibiotics was observed. Furthermore, EGCg inhibited penicillinase activity, thus restoring the antibacterial activity of penicillin against penicillinase-producing S. aureus. The combinations of EGCg with β-lactams against β-lactamase-producing ram-negative rods do indicate a limitation owing to the cellular location of P-lactamases.
Secondly, EGCg alone showed b
… More
actericidal activity against H. pylori with an MIC 100 μg/ml. When EGCg was combined with amoxicillin, metronidazole or clarithromycin, additive effect was observed against highly resistant strains of H. pylori.
Thirdly, the phagocytotic and bactericidal activities of mouse macrophages derived from EGCg-stimulated or-non-stimulated mice by peritoneal injection were detected. EGCg showed an enhancement of both activities in a dose-dependent manner.
Fourthly, the effects of EGCg on HIV were studied. EGCg had a destructive effect on the viral particles and inhibited post-adsorption entry. Both RT and protease was inhibited. Viral production by THP-1 cells (monocyte lineage) chronically-infected with HIV-1 was also inhibited in a dose-dependent manner and the inhibitory effect was enhanced by liposome modification of EGCg as well as combination of EGCg with LPS. However, EGCg did not show the inhibition of viral production from T-lymphoid cells (H9). A weak synergic effect was observed in combination of EGCg with AZT. Less
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