Toxicological impacts of environmentally relevant cadmium concentrations on Staphylococcus epidermidis: insights from integrated metabolomics and transcriptomics

The environmental toxicant cadmium (Cd) can be absorbed by the human body via dermal exposure, yet its influence on skin microbiota remains largely uncharacterized. Staphylococcus epidermidis , a key component of the cutaneous microecosystem, maintains host skin health. This study investigated the interaction between environmentally relevant Cd concentrations and this commensal bacterium, assessing S. epidermidis ’ potential barrier function in Cd–skin crosstalk. Exposure to 0.001 mg/L Cd (estimated urban skin exposure level) for 24 h did not significantly inhibit bacterial growth. However, when Cd concentration exceeded 1 mg/L (estimated highly polluted or occupational exposure level), growth inhibition exhibited a dose‑dependent pattern. This isolate exhibited substantial Cd removal capacity, with a maximal removal rate of 94.4% at 3 mg/L Cd. While 0.001 mg/L Cd induced reactive oxygen species (ROS) generation, it did not affect cell proliferation, protein synthesis, or membrane integrity. In contrast, 1 mg/L Cd elicited a significant ROS burst and upregulated antioxidant enzyme activities, compromising proliferation and altering biochemical composition. Multi-omics analyses revealed a concentration-dependent adaptive strategy: under 0.001 mg/L Cd stress, bacteria activated low-cost survival pathways, including metal sensing, iron competition, ROS detoxification, and membrane homeostasis. Under 1 mg/L Cd exposure, augmented Cd chelation and efflux mechanisms, alongside an elevated metabolic burden, partially inhibited proliferation. S. epidermidis effectively mitigates Cd stress at environmentally relevant concentrations, potentially attenuating direct Cd toxicity to cutaneous cells. This study elucidates novel molecular mechanisms governing beneficial skin bacteria’s response to heavy metal exposure and provides a foundation for evaluating environmental pollutant risk to host health via skin microbiota modulation.