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Staphylococcus aureus autoinducer-2 quorum sensing decreases biofilm formation in an icaR-dependent manner.

Yu D, Zhao L, Xue T, Sun B - BMC Microbiol. (2012)

Bottom Line: Our data indicate a cumulative effect of the two QS systems on the regulation of biofilm formation in S. aureus.These findings demonstrate that AI-2 can decrease biofilm formation in S. aureus via an icaR-activation pathway.This study may provide clues for therapy in S. aureus biofilm-associated infection.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Microbiology and Immunology, School of Life Sciences, University of Science and Technology of China, Hefei, Anhui, China.

ABSTRACT

Background: Staphylococcus aureus is an important pathogen that causes biofilm-associated infection in humans. Autoinducer 2 (AI-2), a quorum-sensing (QS) signal for interspecies communication, has a wide range of regulatory functions in both Gram-positive and Gram-negative bacteria, but its exact role in biofilm formation in S. aureus remains unclear.

Results: Here we demonstrate that mutation of the AI-2 synthase gene luxS in S. aureus RN6390B results in increased biofilm formation compared with the wild-type (WT) strain under static, flowing and anaerobic conditions and in a mouse model. Addition of the chemically synthesized AI-2 precursor in the luxS mutation strain (ΔluxS) restored the WT phenotype. Real-time RT-PCR analysis showed that AI-2 activated the transcription of icaR, a repressor of the ica operon, and subsequently a decreased level of icaA transcription, which was presumably the main reason why luxS mutation influences biofilm formation. Furthermore, we compared the roles of the agr-mediated QS system and the LuxS/AI-2 QS system in the regulation of biofilm formation using the ΔluxS strain, RN6911 and the Δagr ΔluxS strain. Our data indicate a cumulative effect of the two QS systems on the regulation of biofilm formation in S. aureus.

Conclusion: These findings demonstrate that AI-2 can decrease biofilm formation in S. aureus via an icaR-activation pathway. This study may provide clues for therapy in S. aureus biofilm-associated infection.

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Related in: MedlinePlus

Biofilm formation of S. aureus in vivo.  Biofilm formation was assessed using a murine catheter-associated model of WT (NCTC8325) and ΔluxS (NCTC8325ΔluxS). Overnight culture of 5 × 107 CFU was injected into the catheters, which were implanted subcutaneously in the dorsal area of the mice. Results shown are the number of bacteria counted from the catheters after incubation for 3 days. Each point stands for one independent mouse. P value refers to a comparison between WT and ΔluxS and means statistically significant differences (P = 0.001) by Student's t test.
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Figure 3: Biofilm formation of S. aureus in vivo. Biofilm formation was assessed using a murine catheter-associated model of WT (NCTC8325) and ΔluxS (NCTC8325ΔluxS). Overnight culture of 5 × 107 CFU was injected into the catheters, which were implanted subcutaneously in the dorsal area of the mice. Results shown are the number of bacteria counted from the catheters after incubation for 3 days. Each point stands for one independent mouse. P value refers to a comparison between WT and ΔluxS and means statistically significant differences (P = 0.001) by Student's t test.

Mentions: To further verify the effect of AI-2 on biofilm formation in vivo, a murine model of catheter-associated biofilm formation was used. In this assay, mice were separately infected with 5 × 107 CFU/ml of the WT strain and the ΔluxS strain. After incubation for 3 days, the catheters were taken out and the number of bacteria was counted. As shown in Figure 3, the ΔluxS strain exhibited significantly increased capacity to form biofilms compared to the WT strain (P = 0.001) in vivo. These results suggest that LuxS/AI-2 system is involved in the regulation of biofilm formation in vivo, which is consistent with the conclusion in vitro.


Staphylococcus aureus autoinducer-2 quorum sensing decreases biofilm formation in an icaR-dependent manner.

Yu D, Zhao L, Xue T, Sun B - BMC Microbiol. (2012)

Biofilm formation of S. aureus in vivo.  Biofilm formation was assessed using a murine catheter-associated model of WT (NCTC8325) and ΔluxS (NCTC8325ΔluxS). Overnight culture of 5 × 107 CFU was injected into the catheters, which were implanted subcutaneously in the dorsal area of the mice. Results shown are the number of bacteria counted from the catheters after incubation for 3 days. Each point stands for one independent mouse. P value refers to a comparison between WT and ΔluxS and means statistically significant differences (P = 0.001) by Student's t test.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3539994&req=5

Figure 3: Biofilm formation of S. aureus in vivo. Biofilm formation was assessed using a murine catheter-associated model of WT (NCTC8325) and ΔluxS (NCTC8325ΔluxS). Overnight culture of 5 × 107 CFU was injected into the catheters, which were implanted subcutaneously in the dorsal area of the mice. Results shown are the number of bacteria counted from the catheters after incubation for 3 days. Each point stands for one independent mouse. P value refers to a comparison between WT and ΔluxS and means statistically significant differences (P = 0.001) by Student's t test.
Mentions: To further verify the effect of AI-2 on biofilm formation in vivo, a murine model of catheter-associated biofilm formation was used. In this assay, mice were separately infected with 5 × 107 CFU/ml of the WT strain and the ΔluxS strain. After incubation for 3 days, the catheters were taken out and the number of bacteria was counted. As shown in Figure 3, the ΔluxS strain exhibited significantly increased capacity to form biofilms compared to the WT strain (P = 0.001) in vivo. These results suggest that LuxS/AI-2 system is involved in the regulation of biofilm formation in vivo, which is consistent with the conclusion in vitro.

Bottom Line: Our data indicate a cumulative effect of the two QS systems on the regulation of biofilm formation in S. aureus.These findings demonstrate that AI-2 can decrease biofilm formation in S. aureus via an icaR-activation pathway.This study may provide clues for therapy in S. aureus biofilm-associated infection.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Microbiology and Immunology, School of Life Sciences, University of Science and Technology of China, Hefei, Anhui, China.

ABSTRACT

Background: Staphylococcus aureus is an important pathogen that causes biofilm-associated infection in humans. Autoinducer 2 (AI-2), a quorum-sensing (QS) signal for interspecies communication, has a wide range of regulatory functions in both Gram-positive and Gram-negative bacteria, but its exact role in biofilm formation in S. aureus remains unclear.

Results: Here we demonstrate that mutation of the AI-2 synthase gene luxS in S. aureus RN6390B results in increased biofilm formation compared with the wild-type (WT) strain under static, flowing and anaerobic conditions and in a mouse model. Addition of the chemically synthesized AI-2 precursor in the luxS mutation strain (ΔluxS) restored the WT phenotype. Real-time RT-PCR analysis showed that AI-2 activated the transcription of icaR, a repressor of the ica operon, and subsequently a decreased level of icaA transcription, which was presumably the main reason why luxS mutation influences biofilm formation. Furthermore, we compared the roles of the agr-mediated QS system and the LuxS/AI-2 QS system in the regulation of biofilm formation using the ΔluxS strain, RN6911 and the Δagr ΔluxS strain. Our data indicate a cumulative effect of the two QS systems on the regulation of biofilm formation in S. aureus.

Conclusion: These findings demonstrate that AI-2 can decrease biofilm formation in S. aureus via an icaR-activation pathway. This study may provide clues for therapy in S. aureus biofilm-associated infection.

Show MeSH
Related in: MedlinePlus