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

Tan X, Qin N, Wu C, Sheng J, Yang R, Zheng B, Ma Z, Liu L, Peng X, Jia A - Sci Rep (2015)

Bottom Line: 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.

View Article: PubMed Central - PubMed

Affiliation: School of Environmental and Biological Engineering, Nanjing University of Science and Technology, Nanjing 210094, China.

ABSTRACT
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.

No MeSH data available.


Related in: MedlinePlus

Heatmap of differentially expressed genes associated with S. aureus ATCC25923 biofilm formation and virulence.(a) ursolic acid inhibiting S. aureus ATCC25923 biofilm formation condition, (b) resveratrol inhibiting S. aureus ATCC25923 biofilm formation condition, (c) resveratrol removing established S. aureus ATCC25923 biofilm condition, and (d) the mixture of resveratrol and vancomycin removing established S. aureus ATCC25923 biofilm condition.
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f2: Heatmap of differentially expressed genes associated with S. aureus ATCC25923 biofilm formation and virulence.(a) ursolic acid inhibiting S. aureus ATCC25923 biofilm formation condition, (b) resveratrol inhibiting S. aureus ATCC25923 biofilm formation condition, (c) resveratrol removing established S. aureus ATCC25923 biofilm condition, and (d) the mixture of resveratrol and vancomycin removing established S. aureus ATCC25923 biofilm condition.

Mentions: Notably, the sets of genes were highly up-regulated and down-regulated in both conditions including some key known genes encoding virulence factors, surface proteins, proteases, and adhesins, which are related to S. aureus biofilm formation. In the sample that ursolic acid was used to inhibit MSSA biofilm formation (2U30), 69 detected transcripts showed high similarity to known S. aureus genes, many of which were known to be associated with S. aureus biofilm formation (Supplementary Table S2 online, Fig. 2a). icaR, inhibiting ica-dependent biofilm formation in S. aureus, was up-regulated by 4.6-fold compared to control. The expressions of genes (isaA, isaB, clpP, and clpX) encoding proteases IsaA, IsaB, ClpP, and ClpX increased by 4.4, 2.9, 2.8, and 2.3-fold, respectively. The expression of sarX, a sarA paralog, increased by 9.5-fold. Moreover, treatment of ursolic acid increased the expression levels of genes that encode adhesins and surface proteins (fib, map, sdrC, sdrD, and spa) by 2.3, 13.2, 10.7, 5.2, and 5.4-fold, respectively, when MSSA biofilm formation was inhibited. However, the expression of hld gene encoding δ-hemolysin, a surfactant and an important element of S. aureus agr system, decreased 2.6-fold, which was different from the observation in MRSA biofilm of which ursolic acid is also inhibitive18.


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

Tan X, Qin N, Wu C, Sheng J, Yang R, Zheng B, Ma Z, Liu L, Peng X, Jia A - Sci Rep (2015)

Heatmap of differentially expressed genes associated with S. aureus ATCC25923 biofilm formation and virulence.(a) ursolic acid inhibiting S. aureus ATCC25923 biofilm formation condition, (b) resveratrol inhibiting S. aureus ATCC25923 biofilm formation condition, (c) resveratrol removing established S. aureus ATCC25923 biofilm condition, and (d) the mixture of resveratrol and vancomycin removing established S. aureus ATCC25923 biofilm condition.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4493712&req=5

f2: Heatmap of differentially expressed genes associated with S. aureus ATCC25923 biofilm formation and virulence.(a) ursolic acid inhibiting S. aureus ATCC25923 biofilm formation condition, (b) resveratrol inhibiting S. aureus ATCC25923 biofilm formation condition, (c) resveratrol removing established S. aureus ATCC25923 biofilm condition, and (d) the mixture of resveratrol and vancomycin removing established S. aureus ATCC25923 biofilm condition.
Mentions: Notably, the sets of genes were highly up-regulated and down-regulated in both conditions including some key known genes encoding virulence factors, surface proteins, proteases, and adhesins, which are related to S. aureus biofilm formation. In the sample that ursolic acid was used to inhibit MSSA biofilm formation (2U30), 69 detected transcripts showed high similarity to known S. aureus genes, many of which were known to be associated with S. aureus biofilm formation (Supplementary Table S2 online, Fig. 2a). icaR, inhibiting ica-dependent biofilm formation in S. aureus, was up-regulated by 4.6-fold compared to control. The expressions of genes (isaA, isaB, clpP, and clpX) encoding proteases IsaA, IsaB, ClpP, and ClpX increased by 4.4, 2.9, 2.8, and 2.3-fold, respectively. The expression of sarX, a sarA paralog, increased by 9.5-fold. Moreover, treatment of ursolic acid increased the expression levels of genes that encode adhesins and surface proteins (fib, map, sdrC, sdrD, and spa) by 2.3, 13.2, 10.7, 5.2, and 5.4-fold, respectively, when MSSA biofilm formation was inhibited. However, the expression of hld gene encoding δ-hemolysin, a surfactant and an important element of S. aureus agr system, decreased 2.6-fold, which was different from the observation in MRSA biofilm of which ursolic acid is also inhibitive18.

Bottom Line: 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.

View Article: PubMed Central - PubMed

Affiliation: School of Environmental and Biological Engineering, Nanjing University of Science and Technology, Nanjing 210094, China.

ABSTRACT
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.

No MeSH data available.


Related in: MedlinePlus