Pulmonary toxicity and antibiotic resistance risks induced by environmental MRSA exposure in mice.

Methicillin-resistant Staphylococcus aureus (MRSA) is widely present in the air, and its pathogenicity and antibiotic resistance pose potential health threats to humans. The lungs are connected to the external environment through the upper respiratory tract, making them vulnerable to MRSA infection. This study focused on the health risks of airborne MRSA in chicken farm environments and the effects of antibiotic intervention, and conducted in vitro and in vivo experimental studies. In vitro, BEAS-2B cells were used as a model to investigate the effects of MRSA on cell viability, invasion, adhesion, and barrier function; in vivo, a mouse infection model was established to compare the short-term treatment effects of penicillin (resistant) and vancomycin (sensitive). Combined with the analysis of inflammatory indicators and sequencing, the study found that MRSA activated the IL-17 pathway to induce acute pulmonary inflammation; penicillin increased the abundance of pathogenic bacteria in the lungs, while vancomycin was more effective in reducing pulmonary MRSA load, downregulating the expression of key genes in the IL-17 pathway, and alleviating inflammation. This study systematically revealed the acute pulmonary toxicity of environmentally derived MRSA and the key impact of its antibiotic resistance on short-term treatment efficacy, providing an important experimental basis for the in-depth understanding of health risks caused by MRSA.