Inhibition of bacterial growth by antibiotics: a minimal model.

IF 1.5 4区生物学 Q4 BIOCHEMISTRY & MOLECULAR BIOLOGY

Physical biology Pub Date : 2025-10-24 DOI:10.1088/1478-3975/ae1343

Barnabé Ledoux, David Lacoste

引用次数: 0

Abstract

Growth in bacterial populations generally depends on the environment (availability and quality of nutrients, presence of a toxic inhibitor, product inhibition..). Here, we build a minimal model to describe the action of a bacteriostatic antibiotic, assuming that this drug inhibits an essential autocatalytic cycle of the cell metabolism. The model recovers known growth laws, can describe various types of antibiotics and confirms the existence of two distinct regimes of growth-dependent susceptibility, previously identified only for ribosome targeting antibiotics. We introduce a proxy for cell risk, which proves useful to compare the effects of various types of antibiotics. We also develop extensions of our model to describe the effect of combining two antibiotics targeting two different autocatalytic cycles or a regime where cell growth is inhibited by a waste product.

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抗生素对细菌生长的抑制：一个最小模型。

细菌种群的生长通常取决于环境（营养物质的可用性和质量、有毒抑制剂的存在、产物抑制……）。在这里，我们建立了一个最小模型来描述抑菌抗生素的作用，假设这种药物抑制细胞代谢的基本自催化循环。该模型恢复了已知的生长规律，可以描述各种类型的抗生素，并证实了两种不同的生长依赖性敏感性机制的存在，这两种机制以前仅用于靶向抗生素的核糖体。我们介绍了细胞风险的代理，这被证明是有用的，以比较各种类型的抗生素的影响。我们还开发了我们的模型的扩展，以描述针对两种不同的自催化循环或废物抑制细胞生长的制度结合两种抗生素的效果。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Physical biology 生物-生物物理

CiteScore

4.20

自引率

0.00%

发文量

审稿时长

3 months

期刊介绍： Physical Biology publishes articles in the broad interdisciplinary field bridging biology with the physical sciences and engineering. This journal focuses on research in which quantitative approaches – experimental, theoretical and modeling – lead to new insights into biological systems at all scales of space and time, and all levels of organizational complexity. Physical Biology accepts contributions from a wide range of biological sub-fields, including topics such as: molecular biophysics, including single molecule studies, protein-protein and protein-DNA interactions subcellular structures, organelle dynamics, membranes, protein assemblies, chromosome structure intracellular processes, e.g. cytoskeleton dynamics, cellular transport, cell division systems biology, e.g. signaling, gene regulation and metabolic networks cells and their microenvironment, e.g. cell mechanics and motility, chemotaxis, extracellular matrix, biofilms cell-material interactions, e.g. biointerfaces, electrical stimulation and sensing, endocytosis cell-cell interactions, cell aggregates, organoids, tissues and organs developmental dynamics, including pattern formation and morphogenesis physical and evolutionary aspects of disease, e.g. cancer progression, amyloid formation neuronal systems, including information processing by networks, memory and learning population dynamics, ecology, and evolution collective action and emergence of collective phenomena.