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滤过物与伏立康唑对囊性纤维化患者黏液型分离株生物膜的协同作用较低。

Synergy Between Filtrates And Voriconazole Against Biofilm Is Less for Mucoid Isolates From Persons With Cystic Fibrosis.

机构信息

Infectious Disease Research Laboratory, California Institute for Medical Research, San Jose, CA, United States.

Department of Infectious Diseases, National Institute of Health, 'Dr. Ricardo Jorge', Lisbon, Portugal.

出版信息

Front Cell Infect Microbiol. 2022 Apr 14;12:817315. doi: 10.3389/fcimb.2022.817315. eCollection 2022.

DOI:10.3389/fcimb.2022.817315
PMID:35493738
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9047052/
Abstract

Persons with cystic fibrosis (CF) frequently suffer from and co-infections. There is evidence that co-infections with these interacting pathogens cause airway inflammation and aggravate deterioration of lung function. We recently showed that laboratory isolates synergistically interact with the anti-fungal azole voriconazole (VCZ), inhibiting biofilm metabolism of several laboratory strains. Interaction was usually mediated pyoverdine, but also pyocyanin or pyochelin. Here we used planktonic filtrates of 7 mucoid and 9 non-mucoid isolates from CF patients, as well as 8 isolates without CF origin, and found that all of these isolates interacted with VCZ synergistically at their IC50 as well as higher dilutions. CF mucoid isolates showed the weakest interactive effects. Four non-mucoid CF isolates produced no or very low levels of pyoverdine and did not reach an IC50 against forming biofilm; interaction with VCZ still was synergistic. A VCZ-resistant strain showed the same level of susceptibility for anti-fungal activity as a VCZ-susceptible reference strain. Filtrates of most isolates were able to increase anti-fungal activity of VCZ on a susceptible strain. This was also possible for the VCZ-resistant strain. In summary these data show that clinical isolates, at varying degrees, synergistically interact with VCZ, and that pyoverdine is not the only molecule responsible. These data also strengthen the idea that during co-infections of and lower concentrations of VCZ might be sufficient to control fungal growth.

摘要

囊性纤维化（CF）患者经常患有 和 合并感染。有证据表明，这些相互作用的病原体的合并感染会引起气道炎症并加重肺功能恶化。我们最近表明， 实验室分离株与抗真菌唑 voriconazole（VCZ）协同相互作用，抑制几种 实验室菌株的生物膜代谢。相互作用通常由 绿脓菌素介导，但也由 吡咯菌素或焦脱镁叶绿酸介导。在这里，我们使用了来自 CF 患者的 7 株粘液和 9 株非粘液 分离株的浮游滤液，以及 8 株非 CF 来源的分离株，发现所有这些分离株在其 IC50 及更高稀释度下与 VCZ 协同作用。CF 粘液分离株显示出最弱的相互作用效果。4 株非粘液 CF 分离株不产生或仅产生少量绿脓菌素，且未达到形成 生物膜的 IC50；与 VCZ 的相互作用仍具有协同性。VCZ 耐药株对 抗真菌活性的敏感性与 VCZ 敏感的参考株相同。大多数 分离株的滤液能够增加 VCZ 对敏感 株的抗真菌活性。VCZ 耐药株也可以。总之，这些数据表明临床 分离株在不同程度上与 VCZ 协同作用，并且绿脓菌素不是唯一负责的分子。这些数据还加强了这样一种观点，即在 和 的合并感染中，较低浓度的 VCZ 可能足以控制真菌生长。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3042/9047052/fb6022cef71c/fcimb-12-817315-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3042/9047052/57c0bb3186a1/fcimb-12-817315-g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3042/9047052/38c0e23bc7ba/fcimb-12-817315-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3042/9047052/bd4120b80897/fcimb-12-817315-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3042/9047052/03b13a7c061b/fcimb-12-817315-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3042/9047052/fb6022cef71c/fcimb-12-817315-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3042/9047052/57c0bb3186a1/fcimb-12-817315-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3042/9047052/706faf8a3294/fcimb-12-817315-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3042/9047052/06b35df7aead/fcimb-12-817315-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3042/9047052/79174b218c45/fcimb-12-817315-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3042/9047052/bca001f8d56f/fcimb-12-817315-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3042/9047052/129c8ac1985f/fcimb-12-817315-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3042/9047052/38c0e23bc7ba/fcimb-12-817315-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3042/9047052/bd4120b80897/fcimb-12-817315-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3042/9047052/03b13a7c061b/fcimb-12-817315-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3042/9047052/fb6022cef71c/fcimb-12-817315-g010.jpg

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