Department of Microbiology, Hospital Universitario Ramón y Cajal, Instituto Ramón y Cajal de Investigación Sanitaria Madrid, Spain ; Centros de Investigación Biomédica en Red de Epidemiología y Salud Pública Madrid, Spain ; Unidad de Resistencia a Antibióticos y Virulencia Bacteriana asociada al Consejo Superior de Investigaciones Científicas Madrid, Spain.
Front Microbiol. 2013 Mar 6;4:15. doi: 10.3389/fmicb.2013.00015. eCollection 2013.
Antibiotics have natural functions, mostly involving cell-to-cell signaling networks. The anthropogenic production of antibiotics, and its release in the microbiosphere results in a disturbance of these networks, antibiotic resistance tending to preserve its integrity. The cost of such adaptation is the emergence and dissemination of antibiotic resistance genes, and of all genetic and cellular vehicles in which these genes are located. Selection of the combinations of the different evolutionary units (genes, integrons, transposons, plasmids, cells, communities and microbiomes, hosts) is highly asymmetrical. Each unit of selection is a self-interested entity, exploiting the higher hierarchical unit for its own benefit, but in doing so the higher hierarchical unit might acquire critical traits for its spread because of the exploitation of the lower hierarchical unit. This interactive trade-off shapes the population biology of antibiotic resistance, a composed-complex array of the independent "population biologies." Antibiotics modify the abundance and the interactive field of each of these units. Antibiotics increase the number and evolvability of "clinical" antibiotic resistance genes, but probably also many other genes with different primary functions but with a resistance phenotype present in the environmental resistome. Antibiotics influence the abundance, modularity, and spread of integrons, transposons, and plasmids, mostly acting on structures present before the antibiotic era. Antibiotics enrich particular bacterial lineages and clones and contribute to local clonalization processes. Antibiotics amplify particular genetic exchange communities sharing antibiotic resistance genes and platforms within microbiomes. In particular human or animal hosts, the microbiomic composition might facilitate the interactions between evolutionary units involved in antibiotic resistance. The understanding of antibiotic resistance implies expanding our knowledge on multi-level population biology of bacteria.
抗生素具有天然功能，主要涉及细胞间信号网络。抗生素的人为生产及其在微生物圈中的释放会干扰这些网络，而抗生素耐药性则倾向于保持其完整性。这种适应的代价是抗生素耐药基因的出现和传播，以及这些基因所在的所有遗传和细胞载体。不同进化单位（基因、整合子、转座子、质粒、细胞、群落和微生物组、宿主）的组合选择具有高度的不对称性。每个选择单位都是一个自身利益的实体，利用更高层次的单位为自己谋取利益，但这样做可能会使更高层次的单位获得其传播的关键特征，因为它利用了较低层次的单位。这种互动的权衡塑造了抗生素耐药性的群体生物学，这是一个由独立的“群体生物学”组成的复杂组合。抗生素会改变这些单位的丰度和相互作用的范围。抗生素增加了“临床”抗生素耐药基因的数量和可进化性，但也可能增加了许多其他具有不同主要功能但在环境耐药组中具有耐药表型的基因。抗生素影响整合子、转座子和质粒的丰度、模块性和传播，主要作用于抗生素时代之前存在的结构。抗生素使特定的细菌谱系和克隆丰富，并有助于局部克隆化过程。抗生素放大了特定的遗传交换社区，在微生物组内共享抗生素耐药基因和平台。特别是在人类或动物宿主中，微生物组的组成可能有助于参与抗生素耐药性的进化单位之间的相互作用。对抗生素耐药性的理解意味着扩大我们对细菌多层次群体生物学的认识。
