2-Aminoimidazoles Inhibit Mycobacterium abscessus Biofilms in a Zinc-Dependent Manner.
2-Aminoimidazoles Inhibit Mycobacterium abscessus Biofilms in a Zinc-Dependent Manner.
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DOI：
10.3390/ijms23062950
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发表时间：
2022-03-09
影响因子：
5.6
通讯作者：
Jackson M
中科院分区：
文献类型：
--
作者：
Belardinelli JM;Li W;Martin KH;Zeiler MJ;Lian E;Avanzi C;Wiersma CJ;Nguyen TV;Angala B;de Moura VCN;Jones V;Borlee BR;Melander C;Jackson M
生物膜生长被认为是成功治疗结核分枝杆菌感染的重要障碍。寻找能够抑制M. Becomessus生物膜引起了我们对2-氨基咪唑和相关支架的兴趣，这些支架已被证明对许多革兰氏阴性和革兰氏阳性细菌（包括结核分枝杆菌和耻垢分枝杆菌）显示出抗膜特性。对30种化合物的文库的筛选导致鉴定出抑制M. IC 50（抑制50%生物膜形成所需的浓度）在12.5至25 μM范围内。有趣的是，AB-2-29似乎螯合锌，并且通过向培养基中添加锌来增强其抗氧化膜活性。初步的机理研究表明，AB-2-29通过一个不同的机制，从那些迄今报道的2-氨基咪唑化合物的行为。
Biofilm growth is thought to be a significant obstacle to the successful treatment of Mycobacterium abscessus infections. A search for agents capable of inhibiting M. abscessus biofilms led to our interest in 2-aminoimidazoles and related scaffolds, which have proven to display antibiofilm properties against a number of Gram-negative and Gram-positive bacteria, including Mycobacterium tuberculosis and Mycobacterium smegmatis. The screening of a library of 30 compounds led to the identification of a compound, AB-2-29, which inhibits the formation of M. abscessus biofilms with an IC50 (the concentration required to inhibit 50% of biofilm formation) in the range of 12.5 to 25 μM. Interestingly, AB-2-29 appears to chelate zinc, and its antibiofilm activity is potentiated by the addition of zinc to the culture medium. Preliminary mechanistic studies indicate that AB-2-29 acts through a distinct mechanism from those reported to date for 2-aminoimidazole compounds.
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影响因子：
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作者：
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