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首页> 外文期刊>Microbial Pathogenesis >Antimicrobial activities of peptide Cbf-K-16 against drug-resistant Helicobacter pylori infection in vitro and in vivo
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Antimicrobial activities of peptide Cbf-K-16 against drug-resistant Helicobacter pylori infection in vitro and in vivo

机译：肽CBF-K-16对耐药幽门螺杆菌感染肽CBF-K-16体外抗菌活性的抗菌活性

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Helicobacter pylori (H. pylori) infection is highly prevalent, and has developed antimicrobial resistance to virtually all existing antibiotics. Currently, treatment of H. pylori infection (involving proton pump inhibitors and broad-spectrum antibiotics) is suboptimal, with high failure rates. Thus, there is a pressing need to develop new anti-H. pylori therapies. Cbf-K-16, a cathelicidin-like antimicrobial peptide, presented broad antimicrobial activity during our previous research. This study further evaluated the therapeutic potential and the mode of action underlying Cbf-K-16 against clarithromycin- and amoxicillin-resistant H. pylori SS1. The MIC and MBC of Cbf-K-16 against the tested H. pylori were 16 and 32 mu g/ml, respectively, and its killing kinetics was time-dependent, reflecting the thorough elimination of drug-resistant bacteria within 24 h. This peptide also protected H. pylori-infected gastric epithelial cells (GES-1) from death by reducing the cell supernatant and intracellular bacterial counts by 1.9 and 2.9-log(10) units, respectively. These data indicated the powerful antimicrobial effects of Cbf-K-16 in vitro. Meanwhile, notable antimicrobial activity in the mouse gastritis model was observed, with decreasing bacterial counts by 3.9-log(10), units in stomach tissues and Cbf-K-16 could effectively suppress the secretion of inflammatory cytokine IL-8. For its mode of action, Cbf-K-16 not only neutralized the negative potential and increased the membrane uptake of NPN and PI by 78.5% and 85.1%, respectively, but also bound to genomic DNA, which in turn downregulated the expression of adhesion genes (alpA and alpB) and virulence gene (cagA), indicating its effective activities on membrane disruption, DNA-binding and gene expression. The data above demonstrated that Cbf-K-16 possessed effective antimicrobial and anti-inflammatory activities and downregulated the expression of adhesion- and cytotoxin-associated genes of drug-resistant H. pylori SS1, making it a potential candidate for anti-infective therapy.
机译：幽门螺杆菌（H. Pylori）感染率高普遍，并且对几乎所有现有的抗生素产生了抗微生物抗性。目前，H.幽门螺杆菌感染（涉及质子泵抑制剂和广谱抗生素）的治疗是次优的，具有高失效率。因此，迫切需要开发新的抗H.幽门疗法。 CBF-K-16是一种类似于水癌素的抗微生物肽，在我们以前的研究期间呈现了广泛的抗微生物活性。该研究进一步评估了CBF-K-16下面的治疗潜力和作用方式，对克拉霉素和阿莫西林抗性H.Pylori SS1。 CBF-K-16的MIC和MBC对测试的H.Pylori分别为16和32μg/ mL，其杀伤动力学是时间依赖性的，反映了24小时内彻底消除耐药细菌。该肽通过将细胞上清液和细胞内细菌计数分别通过1.9和2.9-log（10）单位分别通过减少细胞上清液和细胞内细菌计数，该肽也受到影响，从死亡中受到保护。这些数据表明了CBF-K-16体外的强烈抗微生物效应。同时，观察到小鼠胃炎模型中的显着抗微生物活性，通过3.9-log（10），细菌计数降低，胃组织和CBF-k-16的单位可以有效地抑制炎症细胞因子IL-8的分泌。对于其作用方式，CBF-K-16不仅将负电位中和，并且分别将NPN和Pi的膜摄取分别增加了78.5％和85.1％，而且还与基因组DNA结合，这反过来又称粘附的表达基因（ALPA和ALPB）和毒力基因（CAGA），表明其对膜破坏，DNA结合和基因表达的有效活性。上述数据证明CBF-K-16具有有效的抗微生物和抗炎活动，并下调了耐药H.Pylori SS1的粘附和细胞毒素相关基因的表达，使其成为抗感染治疗的潜在候选者。

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