期刊名称:Proceedings of the National Academy of Sciences
印刷版ISSN:0027-8424
电子版ISSN:1091-6490
出版年度:2022
卷号:119
期号:22
DOI:10.1073/pnas.2118361119
语种:English
出版社:The National Academy of Sciences of the United States of America
摘要:Significance
Antimicrobial resistance (AMR) poses a great challenge for modern medicine. Plasmids are important vectors of antibiotic resistance genes. Plasmids can have context-dependent effects on their hosts, generally slowing their growth rate but also providing protection from specific antibiotics and heavy metals. Thus, models that predict population densities based on interactions between species are useful for explaining plasmid dynamics. Here, we predict with a simple ecological model the properties of a host (e.g., bacteria) and symbiont (e.g., plasmid) interaction network. Using experimental microbial communities and a conjugative plasmid, we confirm our predictions that beneficial symbionts spread more widely through a microbial community and provide key experimental results for network ecologists seeking to uncover the determinants of ecological network structure.
Antimicrobial resistance (AMR) genes are often carried on broad host range plasmids, and the spread of AMR within microbial communities will therefore depend on the structure of bacteria–plasmid networks. Empirical and theoretical studies of ecological interaction networks suggest that network structure differs between communities that are predominantly mutualistic versus antagonistic, with the former showing more generalized interactions (i.e., species interact with many others to a similar extent). This suggests that mutualistic bacteria–plasmid networks—where antibiotics are present and plasmids carry AMR genes—will be more generalized than antagonistic interactions, where plasmids do not confer benefits to their hosts. We first develop a simple theory to explain this link: fitness benefits of harboring a mutualistic symbiont promote the spread of the symbiont to other species. We find support for this theory using an experimental bacteria–symbiont (plasmid) community, where the same plasmid can be mutualistic or antagonistic depending on the presence of antibiotics. This short-term and parsimonious mechanism complements a longer-term mechanism (coevolution and stability) explaining the link between mutualistic and antagonistic interactions and network structure.