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外膜囊泡有助于支气管扩张症患者酸性气道对抗菌肽的抗性。

Outer membrane vesicle contributes to the resistance to antimicrobial peptides in the acidic airway of bronchiectasis patients.

作者信息

Xie Yingzhou, Shi Yi-Han, Wang Le-Le, Li Cheng-Wei, Wu Min, Xu Jin-Fu

机构信息

Shanghai Pulmonary Hospital, Institute of Respiratory Medicine, School of Medicine Tongji University Shanghai China.

Department of Pulmonary and Critical Care Medicine Huashan Hospital, Fudan University Shanghai China.

出版信息

MedComm (2020). 2025 Jan 30;6(2):e70084. doi: 10.1002/mco2.70084. eCollection 2025 Feb.

DOI:10.1002/mco2.70084
PMID:39896756
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11782972/
Abstract

is the predominant pathogen causing chronic infection in the airway of patients with bronchiectasis (BE), a chronic respiratory disease with high prevalence worldwide. Environmental factors are vital for bacterial successful colonization. Here, with sputa and bronchoalveolar lavage fluids, we determined that the concentration of airway antimicrobial peptide LL-37 and lactate was elevated in BE patients, especially in those infected with . The in vitro antibacterial assay revealed the bactericidal activity of LL-37 against the clinical isolates, which were dampened in the acidic condition. production of outer membrane vesicles (OMVs) enhanced in the lactate-adjusted acidic condition. Transcriptomic analysis suggested that OMVs induce the hyperproduction of the chemical compound 2-heptyl-4-quinolone (HHQ) in the bacterial population, which was verified by high-performance liquid chromatography. The positively charged HHQ interfered with the binding of LL-37 to bacterial cell membrane, potentiating the resistance to LL-37. To our knowledge, this is a new resistance mechanism of against antimicrobial peptides and may provide theoretical support for the development of new antibacterial therapies.

摘要

是导致支气管扩张症(BE)患者气道慢性感染的主要病原体,支气管扩张症是一种在全球范围内患病率很高的慢性呼吸道疾病。环境因素对于细菌成功定植至关重要。在这里,我们通过痰液和支气管肺泡灌洗液测定发现,BE患者气道抗菌肽LL-37和乳酸的浓度升高,尤其是在那些感染了……的患者中。体外抗菌试验显示LL-37对临床分离株具有杀菌活性,而在酸性条件下这种活性会受到抑制。在乳酸调节的酸性条件下,外膜囊泡(OMV)的产生增强。转录组分析表明,OMV会诱导细菌群体中化合物2-庚基-4-喹诺酮(HHQ)的过量产生,这一点通过高效液相色谱法得到了验证。带正电荷的HHQ会干扰LL-37与细菌细胞膜的结合,增强对LL-37的抗性。据我们所知,这是……对抗菌肽的一种新的抗性机制,可能为新抗菌疗法的开发提供理论支持。 (注:原文中部分内容缺失,翻译时保留了原文的省略部分)

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8514/11782972/fcf1b93a441a/MCO2-6-e70084-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8514/11782972/99ef5f70c0ea/MCO2-6-e70084-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8514/11782972/ac2c32d9b2c9/MCO2-6-e70084-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8514/11782972/773dcf3d470a/MCO2-6-e70084-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8514/11782972/c4c146087fdc/MCO2-6-e70084-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8514/11782972/fcf1b93a441a/MCO2-6-e70084-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8514/11782972/99ef5f70c0ea/MCO2-6-e70084-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8514/11782972/ac2c32d9b2c9/MCO2-6-e70084-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8514/11782972/773dcf3d470a/MCO2-6-e70084-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8514/11782972/c4c146087fdc/MCO2-6-e70084-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8514/11782972/fcf1b93a441a/MCO2-6-e70084-g006.jpg

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