Review demonstrates how heavy metals influence bacterial virulence in Caenorhabditis elegans, indicating health risk implications.
Heavy metal pollution is increasingly recognized, not merely as a source of static toxicity, but also as a driver of dynamic microbial regulation. At sublethal concentrations, these pollutants function as critical environmental cues that reshape microbial evolutionary trajectories. This review elucidates how low-dose heavy metals bypass acute cellular damage to instead engage bacterial chemical-sensing networks, systematically upregulating virulence factors, biofilm architecture, and the co-selection of antibiotic resistance. By leveraging the Caenorhabditis elegans (C. elegans) infection model (a platform defined by its evolutionarily conserved innate immune architecture), we dissect the tripartite interplay between environmental metal flux, bacterial pathogenic output, and host immunological defense. We synthesize empirical evidence from the C. elegans model to highlight how heavy metals modulate bacterial virulence and host defense mechanisms, thereby providing new insights into the indirect health risks of environmental pollutants and their implications for redefining public health exposure thresholds and infectious disease control in the Anthropocene.
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Zhang et al. (2026) studied this question.
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