ArticleBMC genomics2025
Upregulation of metallophore-related genes of community-acquired methicillin-resistant Staphylococcus aureus enhances pathogenicity in BALB/c mice.
Article in BMC genomics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundOur previous study revealed that ST59-t437-SCCmecIVa methicillin-resistant Staphylococcus aureus (MRSA) has strong pathogenicity and can cause damage to host tissue and cell death. However, the interaction between the pathogen and the host during the infection process remains unclear. This study developed an infection interaction model of highly virulent ST59-t437-SCCmecIVa in MRSA and BALB/c mice.
resultsThe results revealed that the lungs were among the main organs involved, with high bacterial loads in the lung tissue of infected mice. WGCNA and Cytoscape analysis revealed that the metallophore-related genes of MRSA associated with the virulence factors of the strain formed an interaction network. Prokaryotic strand-specific RNA-seq analyses in vivo and in vitro further demonstrated that MRSA significantly upregulated metallophore-related genes during infection. The RT-qPCR results for genes such as sbnC, sbnI, cntA, hlgC, sspB, and pknB verified the interaction and pathogenic role of metallophores with virulence genes in the infection model. Animal hosts secrete large amounts of inflammatory mediators during infection, producing a strong inflammatory response that causes extensive hemorrhage and necrosis of host tissue cells. This led to a cytokine storm and ventilation dysfunction of the lung tissue and thus death.
conclusionsIn this study, through the pathogen-host infection interaction model, we thoroughly explored the changes in the gene expression during the interaction process from both the pathogen and the host, as well as the causes of death of the host animals.
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