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π-conjugated microplastics act as hazard amplifiers of antibiotic resistance through cross-kingdom network engineering
Summary
Researchers discovered that polystyrene microplastics with specific chemical properties can amplify antibiotic resistance through a chemistry-driven mechanism rather than simple physical biofilm formation. The microplastics concentrated the signaling molecule indole on their surfaces, which triggered cross-kingdom gene transfer networks that spread resistance genes. The study reveals a previously unknown chemical pathway by which certain microplastics may actively accelerate the spread of antibiotic resistance in the environment.
Microplastics are recognized as environmental vectors for antibiotic resistance genes (ARGs), a role traditionally ascribed to physical mechanisms such as biofilm-enhanced horizontal gene transfer. Here, we uncover a chemistry-driven pathway that fundamentally surpasses the traditional passive vector model. We show that π‑conjugated polystyrene (PS) microplastics serve as powerful chemical hazard amplifyers by specifically concentrating the signaling molecule indole on their surfaces through π-π stacking and electrostatic interactions (binding energy = -128.56 kcal/mol), creating localized interfacial risk hotspots. These hotspots drive the reprogramming of soil microbiomes, as evidenced by distinct transformations in dissolved organic matter (DOM), and promote a cross-kingdom microbial alliance centered on the keystone fungus Pseudeurotium. This fungal hub transmits the amplified indole signal to bacterial degraders, markedly elevating the dissemination risk of clinically relevant ARGs (e.g., sul2). Through an integration of molecular simulations, multi-omics analyses, and causal modeling, our structural equation modeling (SEM) identifies the amplified indole signal as the primary direct driver of ARG abundance (path coefficient β = 0.47)-an effect 23.5 times greater than that of the PS polymer itself. Our findings establish "Chemical Interfacial-Driven Network Engineering (CIDNE)" as a pivotal mechanism, redefining how synthetic materials actively reshape microbial networks and escalate environmental resistome risk through molecular-scale interfacial interactions.