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SCCmec-associated psm-mec mRNA promotes Staphylococcus epidermidis biofilm formation

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Abstract

Biofilm formation is considered the major pathogenic mechanism of Staphylococcus epidermidis-associated nosocomial infections. Reports have shown that SCCmec-associated psm-mec regulated methicillin-resistant Staphylococcus aureus virulence and biofilm formation. However, the role of psm-mec in S. epidermidis remains unclear. To this purpose, we analysed 165 clinical isolates of S. epidermidis to study the distribution, mutation and expression of psm-mec and the relationship between this gene and biofilm formation. Next, we constructed three psm-mec deletion mutants, one psm-mec transgene expression strain (p221) and two psm-mec point mutant strains (pM, pAG) to explore its effects on S. epidermidis biofilm formation. Then, the amount of biofilm formation, extracellular DNA (eDNA) and Triton X-100-induced autolysis of the constructed strains was measured. Results of psm-mec deletion and transgene expression showed that the gene regulated S. epidermidis biofilm formation. Compared with the control strains, the ability to form biofilm, Triton X-100-induced autolysis and the amount of eDNA increased in the p221 strain and the two psm-mec mutants pM and pAG expressed psm-mec mRNA without its protein, whereas no differences were observed among the three constructed strains, illustrating that psm-mec mRNA promoted S. epidermidis biofilm formation through up-regulation of bacterial autolysis and the release of eDNA. Our results reveal that acquisition of psm-mec promotes S. epidermidis biofilm formation.

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Acknowledgments

We thank Li Min from Shanghai Jiaotong University (China), Sun Baolin from the University of Science and Technology of China (China) for providing of strains and plasmid.

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Correspondence to Yibing Yin.

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Yang, Y., Zhang, X., Huang, W. et al. SCCmec-associated psm-mec mRNA promotes Staphylococcus epidermidis biofilm formation. Antonie van Leeuwenhoek 109, 1403–1415 (2016). https://doi.org/10.1007/s10482-016-0741-2

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  • DOI: https://doi.org/10.1007/s10482-016-0741-2

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