Send to

Choose Destination
Sci Rep. 2015 Jul 7;5:11997. doi: 10.1038/srep11997.

Transcriptome analysis of the biofilm formed by methicillin-susceptible Staphylococcus aureus.

Author information

School of Environmental and Biological Engineering, Nanjing University of Science and Technology, Nanjing 210094, China.
State Key Laboratory for Diagnosis and Treatment of Infectious Disease, the First Affiliated Hospital, Zhejiang University, Hangzhou 310003, China.
Realbio Genomics Institute, Shanghai 200050, China.
Kunming Institute of Zoology, Chinese Academy of Science, Kunming 650223, China.
School of Chemical Engineering, Nanjing University of Science and Technology, Nanjing 210094, China.


Biofilm formation is regarded as one of the major determinants in the prevalence of methicillin-resistant Staphylococcus aureus (MRSA) as pathogens of medical device-related infection. However, methicillin-susceptible S. aureus (MSSA) can also form biofilm in vitro and such biofilms are resistant to vancomycin. Hence, researching the possible mechanisms of MSSA biofilm formation is urgent and necessary. Here, we used S. aureus ATCC25923 as the model strain, and studied gene expression profiles in biofilms after the treatment of ursolic acid and resveratrol using RNA-seq technology. The results showed that only ursolic acid could inhibit biofilm formation, which differed from their applied on the multiple clinical drugs resistant MRSA biofilm. RNA-seq data was validated by examining the expression of six genes involved in biofilm formation by qRT-PCR. These data analysis indicated that the mechanism of the MSSA biofilm formation was different from that of the MRSA, due to absence of accessory gene regulator (agr) function. These findings suggest that biofilms of S. aureus with agr dysfunction may be more resistant than those with agr function. Therefore, the infection from clinical MSSA may be recalcitrant once forming biofilm. Further study is necessary to uncover the mechanisms of biofilm formation in other clinical S. aureus.

[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Nature Publishing Group Icon for PubMed Central
Loading ...
Support Center