利用遗传算法模拟微生物组共同进化动力学和生态失调由于环境和药物的压力

Mithra V. Karamchedu
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引用次数: 0

摘要

一些研究已经确立了微生物组在塑造人类健康方面的关键作用。稳态平衡是不同微生物菌落的微生物稳态,是共同进化的结果,影响持续健康、慢性疾病或对不健康的易感性。环境压力因素,包括感染和药物,可以引发这些微生物菌落的不平衡和不适应。由于共同的生物学功能(聚类信号),相关物种的微生物种群往往与特定的生物学结果相关联。同样,不同的相互依赖的物种也与特定的生物学结果(密集信号)有关。当有意或无意的影响破坏了相对稳定的微生物种群时,如果我们要最终了解这种破坏的长期影响,了解这种改变状态下的共同进化动力学是很重要的。本研究试图创建一种通用的方法来模拟微生物组由于外部触发的破坏的共同进化动力学。初步结果表明,该模型成功地模拟了稳定的相对组成,并评估了微生物组物种的成对竞争/合作得分。该结果支持模拟和预测炎症性肠病(IBD)的流行作为共同进化动力学的结果的前景。结果进一步支持了使用这种计算方法来模拟抗生素引起的微生物组破坏的可能性。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Using Genetic Algorithms to Model Microbiome Coevolutionary Dynamics and Dysbiosis Due to Environmental and Pharmaceutical Stressors
Several studies have established the critical role of microbiome in shaping human health. Steady state balance, a microbial homeostasis, of disparate microbial colonies is the outcome of coevolution and affects the continued health, chronic disease or susceptibility to ill-health. Environmental stressors, including infection and pharmaceuticals, can trigger imbalance and maladaptation of these microbial colonies. Microbial populations of related species are often associated with a specific biological outcome due to a shared biological function (clustered signal). Similarly, diverse interdependent species are also associated with a specific biological outcome (dense signal). When either deliberate or inadvertent influences disrupt the stable relative population of microbes, understanding the dynamics of coevolution in the altered state is important if we are to ultimately understand the longer-term effects of such a disruption. This study attempts to create a generalized approach to model the coevolutionary dynamics of the microbiome due externally triggered disruptions. Preliminary results suggest that the model is successful in simulating stable relative compositions and evaluating pair-wise competition/cooperation scores for microbiome species. The results support the prospect of simulating and predicting the prevalence of Inflammatory Bowel Disease (IBD) as a result of co-evolutionary dynamics. The results further support the possibility of using such a computational approach to model antibiotic induced disruptions to the microbiome.
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