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The insect antimicrobial peptide cecropin A disrupts uropathogenic Escherichia coli biofilms.
npj Biofilms and Microbiomes ( IF 9.2 ) Pub Date : 2020-02-12 , DOI: 10.1038/s41522-020-0116-3
Miriam Kalsy 1 , Miray Tonk 2, 3 , Martin Hardt 4 , Ulrich Dobrindt 5 , Agnieszka Zdybicka-Barabas 6 , Malgorzata Cytrynska 6 , Andreas Vilcinskas 1, 2, 3 , Krishnendu Mukherjee 1, 5
Affiliation  

Current antibiotics cannot eradicate uropathogenic Escherichia coli (UPEC) biofilms, leading to recurrent urinary tract infections. Here, we show that the insect antimicrobial peptide cecropin A (CecA) can destroy planktonic and sessile biofilm-forming UPEC cells, either alone or when combined with the antibiotic nalidixic acid (NAL), synergistically clearing infection in vivo without off-target cytotoxicity. The multi-target mechanism of action involves outer membrane permeabilization followed by biofilm disruption triggered by the inhibition of efflux pump activity and interactions with extracellular and intracellular nucleic acids. These diverse targets ensure that resistance to the CecA + NAL combination emerges slowly. The antimicrobial mechanisms of CecA, thus, extend beyond pore-forming activity to include an unanticipated biofilm-eradication process, offering an alternative approach to combat antibiotic-resistant UPEC infections.

中文翻译:

昆虫抗菌肽天蚕素A破坏尿毒症性大肠杆菌生物膜。

当前的抗生素无法根除尿路致病性大肠杆菌(UPEC)生物膜,从而导致尿路感染反复发作。在这里,我们表明,昆虫抗菌肽天蚕素A(CecA)可以单独或与抗生素萘啶酸(NAL)组合使用时破坏浮游生物和无柄生物膜形成UPEC细胞,在体内协同清除感染,而不会产生脱靶细胞毒性。多靶点的作用机制涉及外膜通透性,随后是生物膜的破坏,该破坏是由外排泵活性的抑制以及与细胞外和细胞内核酸的相互作用引发的。这些不同的靶标可确保对CecA + NAL组合的耐药性缓慢出现。因此,CecA的抗菌机制
更新日期:2020-02-12
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