<it>Staphylococcus aureus</it> autoinducer-2 quorum sensing decreases biofilm formation in an <it>icaR</it>-dependent manner
<p>Abstract</p> <p>Background</p> <p><it>Staphylococcus aureus</it> 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...
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doaj-1754f9469d104f959e219b87c3c18f8e2020-11-25T00:27:33ZengBMCBMC Microbiology1471-21802012-12-0112128810.1186/1471-2180-12-288<it>Staphylococcus aureus</it> autoinducer-2 quorum sensing decreases biofilm formation in an <it>icaR</it>-dependent mannerYu DanZhao LipingXue TingSun Baolin<p>Abstract</p> <p>Background</p> <p><it>Staphylococcus aureus</it> 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 <it>S. aureus</it> remains unclear.</p> <p>Results</p> <p>Here we demonstrate that mutation of the AI-2 synthase gene <it>luxS</it> in <it>S. aureus</it> 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 <it>luxS</it> mutation strain (ΔluxS) restored the WT phenotype. Real-time RT-PCR analysis showed that AI-2 activated the transcription of <it>icaR</it>, a repressor of the <it>ica</it> operon, and subsequently a decreased level of <it>icaA</it> transcription, which was presumably the main reason why <it>luxS</it> mutation influences biofilm formation. Furthermore, we compared the roles of the <it>agr</it>-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 <it>S. aureus</it>.</p> <p>Conclusion</p> <p>These findings demonstrate that AI-2 can decrease biofilm formation in <it>S. aureus</it> via an <it>icaR</it>-activation pathway. This study may provide clues for therapy in <it>S. aureus</it> biofilm-associated infection.</p> http://www.biomedcentral.com/1471-2180/12/288 |
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DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Yu Dan Zhao Liping Xue Ting Sun Baolin |
spellingShingle |
Yu Dan Zhao Liping Xue Ting Sun Baolin <it>Staphylococcus aureus</it> autoinducer-2 quorum sensing decreases biofilm formation in an <it>icaR</it>-dependent manner BMC Microbiology |
author_facet |
Yu Dan Zhao Liping Xue Ting Sun Baolin |
author_sort |
Yu Dan |
title |
<it>Staphylococcus aureus</it> autoinducer-2 quorum sensing decreases biofilm formation in an <it>icaR</it>-dependent manner |
title_short |
<it>Staphylococcus aureus</it> autoinducer-2 quorum sensing decreases biofilm formation in an <it>icaR</it>-dependent manner |
title_full |
<it>Staphylococcus aureus</it> autoinducer-2 quorum sensing decreases biofilm formation in an <it>icaR</it>-dependent manner |
title_fullStr |
<it>Staphylococcus aureus</it> autoinducer-2 quorum sensing decreases biofilm formation in an <it>icaR</it>-dependent manner |
title_full_unstemmed |
<it>Staphylococcus aureus</it> autoinducer-2 quorum sensing decreases biofilm formation in an <it>icaR</it>-dependent manner |
title_sort |
<it>staphylococcus aureus</it> autoinducer-2 quorum sensing decreases biofilm formation in an <it>icar</it>-dependent manner |
publisher |
BMC |
series |
BMC Microbiology |
issn |
1471-2180 |
publishDate |
2012-12-01 |
description |
<p>Abstract</p> <p>Background</p> <p><it>Staphylococcus aureus</it> 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 <it>S. aureus</it> remains unclear.</p> <p>Results</p> <p>Here we demonstrate that mutation of the AI-2 synthase gene <it>luxS</it> in <it>S. aureus</it> 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 <it>luxS</it> mutation strain (ΔluxS) restored the WT phenotype. Real-time RT-PCR analysis showed that AI-2 activated the transcription of <it>icaR</it>, a repressor of the <it>ica</it> operon, and subsequently a decreased level of <it>icaA</it> transcription, which was presumably the main reason why <it>luxS</it> mutation influences biofilm formation. Furthermore, we compared the roles of the <it>agr</it>-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 <it>S. aureus</it>.</p> <p>Conclusion</p> <p>These findings demonstrate that AI-2 can decrease biofilm formation in <it>S. aureus</it> via an <it>icaR</it>-activation pathway. This study may provide clues for therapy in <it>S. aureus</it> biofilm-associated infection.</p> |
url |
http://www.biomedcentral.com/1471-2180/12/288 |
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