ID | 110537 |
タイトルヨミ | ヤクザイ タイセイ コクフク ノ タメ ノ アタラシイ ホウホウ : MRSA ニ タイスル β‐ラクタムザイ カンジュセイ ユウドウヤク ILSMR ノ ソウセイ オ メザシテ
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タイトル別表記 | The new method for the drug tolerance conquest : with the aim of the invention of inducer medicine of β-lactam drugs-susceptibility in methicillin-resistant Staphylococcus aureus (ILSMR)
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著者 | |
キーワード | β-lactam drugs-susceptibility
methicillin-resistant Staphylococcus aureus
ILSMR
penicillin binding protein
PBP 2’
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資料タイプ |
学術雑誌論文
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抄録 | Here we demonstrated that flavone and its derivatives had no or week antibacterial effect on methicillin-resistant Staphylococcus aureus (MRSA), but dramatically induced susceptibility to β-lactam antibiotics in most strains of MRSA isolated clinically, even up to a 32,000-fold increase. We named these flavones “inducer of β-lactam drugs-susceptibility in MRSA”, abbreviated as “ILSMR”. We also proposed the model for the mechanism of high resistance of MRSA to β-lactam drugs in which we assumed as follows : ( 1 ) PBP2’ (PBP2A) has low affinity not only to the β-lactam ring in β-lactam drugs, but also to D-Ala-(D)-Ala in N-acetyl-muramyl-pentapeptide and that ( 2 ) PBP 2’ can cross-link between N-acetyl-muramyl-pentapeptide and penta-glycine only when MRSA has been mutated such as the concentrations of these substrates have been greatly increased in the cross wall of staphylococcal cell. Based on the model, we could explain that ILSMRs increased susceptibility to β-lactam drugs in MRSA by decreasing the concentration of N-acetyl-muramyl-pentapeptide and/or penta-glycine in the growing cross wall. In such conditions, only normal PBP1~4 could work for the cross-link. This could be the reason why ILSMRs increased the susceptibility to β-lactam drugs in MRSA. We also found that flavone and its derivatives were highly active against systemic infections by MRSA in mice.
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掲載誌名 |
四国医学雑誌
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ISSN | 00373699
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cat書誌ID | AN00102041
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出版者 | 徳島医学会
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巻 | 58
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号 | 3
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開始ページ | 107
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終了ページ | 121
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並び順 | 107
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発行日 | 2002-06-15
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EDB ID | |
フルテキストファイル | |
言語 |
jpn
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著者版フラグ |
出版社版
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部局 |
薬学系
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