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量化流感期间联合治疗预防细菌合并感染的治疗需求和潜力。

Quantifying the therapeutic requirements and potential for combination therapy to prevent bacterial coinfection during influenza.

作者信息

Smith Amber M

机构信息

Department of Infectious Diseases, St. Jude Children's Research Hospital, Memphis, TN, 38105, USA.

出版信息

J Pharmacokinet Pharmacodyn. 2017 Apr;44(2):81-93. doi: 10.1007/s10928-016-9494-9. Epub 2016 Sep 27.

DOI:10.1007/s10928-016-9494-9
PMID:27679506
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5376398/
Abstract

Secondary bacterial infections (SBIs) exacerbate influenza-associated disease and mortality. Antimicrobial agents can reduce the severity of SBIs, but many have limited efficacy or cause adverse effects. Thus, new treatment strategies are needed. Kinetic models describing the infection process can help determine optimal therapeutic targets, the time scale on which a drug will be most effective, and how infection dynamics will change under therapy. To understand how different therapies perturb the dynamics of influenza infection and bacterial coinfection and to quantify the benefit of increasing a drug's efficacy or targeting a different infection process, I analyzed data from mice treated with an antiviral, an antibiotic, or an immune modulatory agent with kinetic models. The results suggest that antivirals targeting the viral life cycle are most efficacious in the first 2 days of infection, potentially because of an improved immune response, and that increasing the clearance of infected cells is important for treatment later in the infection. For a coinfection, immunotherapy could control low bacterial loads with as little as 20 % efficacy, but more effective drugs would be necessary for high bacterial loads. Antibiotics targeting bacterial replication and administered 10 h after infection would require 100 % efficacy, which could be reduced to 40 % with prophylaxis. Combining immunotherapy with antibiotics could substantially increase treatment success. Taken together, the results suggest when and why some therapies fail, determine the efficacy needed for successful treatment, identify potential immune effects, and show how the regulation of underlying mechanisms can be used to design new therapeutic strategies.

摘要

继发性细菌感染(SBIs)会加剧流感相关疾病并导致死亡。抗菌药物可降低SBIs的严重程度,但许多药物疗效有限或会产生不良反应。因此,需要新的治疗策略。描述感染过程的动力学模型有助于确定最佳治疗靶点、药物最有效作用的时间尺度以及治疗过程中感染动态将如何变化。为了解不同疗法如何扰乱流感感染和细菌合并感染的动态,并量化提高药物疗效或针对不同感染过程的益处,我用动力学模型分析了用抗病毒药、抗生素或免疫调节剂治疗的小鼠的数据。结果表明,针对病毒生命周期的抗病毒药物在感染的头两天最有效,这可能是因为免疫反应得到改善,并且增加被感染细胞的清除率对于感染后期的治疗很重要。对于合并感染,免疫疗法可通过低至20%的疗效控制低细菌载量,但对于高细菌载量则需要更有效的药物。针对细菌复制且在感染后10小时给药的抗生素需要100%的疗效,通过预防可将其降至40%。将免疫疗法与抗生素联合使用可大幅提高治疗成功率。综上所述,这些结果表明了某些疗法何时以及为何失败,确定了成功治疗所需的疗效,识别了潜在的免疫效应,并展示了如何利用对潜在机制的调控来设计新的治疗策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2763/5376398/d34a868dea58/10928_2016_9494_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2763/5376398/a00bdf7cd8f8/10928_2016_9494_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2763/5376398/6270a8821a87/10928_2016_9494_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2763/5376398/b59aa91d00ef/10928_2016_9494_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2763/5376398/c9a6da17a7f0/10928_2016_9494_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2763/5376398/d34a868dea58/10928_2016_9494_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2763/5376398/a00bdf7cd8f8/10928_2016_9494_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2763/5376398/6270a8821a87/10928_2016_9494_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2763/5376398/b59aa91d00ef/10928_2016_9494_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2763/5376398/c9a6da17a7f0/10928_2016_9494_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2763/5376398/d34a868dea58/10928_2016_9494_Fig5_HTML.jpg

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