Identification of <i>cbiO</i> Gene Critical for Biofilm Formation by MRSA CFSa36 Strain Isolated from Pediatric Patient with Cystic Fibrosis

The colonization of <i>Staphylococcus aureus</i>, especially methicillin-resistant <i>S. aureus</i> (MRSA), has a detrimental effect on the respiratory care of pediatric patients with cystic fibrosis (CF). In addition to being resistant to multiple antibiotics, <i>S. au...

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Autores principales: Ying Liu, Junshu Yang, Michelle Ji, James Phillips, Mark Wylam, Yinduo Ji
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Publicado: MDPI AG 2021
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spelling oai:doaj.org-article:5739aaa053d140b2b5a4a2087df980372021-11-25T18:37:38ZIdentification of <i>cbiO</i> Gene Critical for Biofilm Formation by MRSA CFSa36 Strain Isolated from Pediatric Patient with Cystic Fibrosis10.3390/pathogens101113632076-0817https://doaj.org/article/5739aaa053d140b2b5a4a2087df980372021-10-01T00:00:00Zhttps://www.mdpi.com/2076-0817/10/11/1363https://doaj.org/toc/2076-0817The colonization of <i>Staphylococcus aureus</i>, especially methicillin-resistant <i>S. aureus</i> (MRSA), has a detrimental effect on the respiratory care of pediatric patients with cystic fibrosis (CF). In addition to being resistant to multiple antibiotics, <i>S. aureus</i> also has the ability to form biofilms, which makes the infection more difficult to treat and eradicate. In this study, we examined the ability of <i>S. aureus</i> strains isolated from pediatric patients with CF to form biofilms. We screened a transposon mutant library of MRSA and identified a putative cobalt transporter ATP binding domain (<i>cbiO</i>) that is required for biofilm formation. We discovered that deleting <i>cbiO</i> creating a <i>cbiO</i> null mutant in CFSa36 (an MRSA strain isolated from a patient with cystic fibrosis) significantly hinders the ability of CFSa36 to form biofilm. The complementation of <i>cbiO</i> restored the ability of the <i>cbiO</i> deletion mutant to generate biofilm. Interestingly, we revealed that incorporating extra copper ions to the chemically defined medium (CDM) complemented the function of <i>cbiO</i> for biofilm formation in a dose-dependent manner, while the addition of extra iron ions in CDM enhanced the effect of <i>cbiO</i> null mutation on biofilm formation. In addition, neither the addition of certain extra amounts of copper ions nor iron ions in CDM had an impact on bacterial growth. Taken together, our findings suggest that <i>cbiO</i> mediates biofilm formation by affecting the transportation of copper ions in the MRSA CFSa36 strain. This study provides new insights into the molecular basis of biofilm formation by <i>S. aureus</i>.Ying LiuJunshu YangMichelle JiJames PhillipsMark WylamYinduo JiMDPI AGarticle<i>Staphylococcus aureus</i>MRSAbiofilm formation<i>cbiO</i>copper ionsMedicineRENPathogens, Vol 10, Iss 1363, p 1363 (2021)
institution DOAJ
collection DOAJ
language EN
topic <i>Staphylococcus aureus</i>
MRSA
biofilm formation
<i>cbiO</i>
copper ions
Medicine
R
spellingShingle <i>Staphylococcus aureus</i>
MRSA
biofilm formation
<i>cbiO</i>
copper ions
Medicine
R
Ying Liu
Junshu Yang
Michelle Ji
James Phillips
Mark Wylam
Yinduo Ji
Identification of <i>cbiO</i> Gene Critical for Biofilm Formation by MRSA CFSa36 Strain Isolated from Pediatric Patient with Cystic Fibrosis
description The colonization of <i>Staphylococcus aureus</i>, especially methicillin-resistant <i>S. aureus</i> (MRSA), has a detrimental effect on the respiratory care of pediatric patients with cystic fibrosis (CF). In addition to being resistant to multiple antibiotics, <i>S. aureus</i> also has the ability to form biofilms, which makes the infection more difficult to treat and eradicate. In this study, we examined the ability of <i>S. aureus</i> strains isolated from pediatric patients with CF to form biofilms. We screened a transposon mutant library of MRSA and identified a putative cobalt transporter ATP binding domain (<i>cbiO</i>) that is required for biofilm formation. We discovered that deleting <i>cbiO</i> creating a <i>cbiO</i> null mutant in CFSa36 (an MRSA strain isolated from a patient with cystic fibrosis) significantly hinders the ability of CFSa36 to form biofilm. The complementation of <i>cbiO</i> restored the ability of the <i>cbiO</i> deletion mutant to generate biofilm. Interestingly, we revealed that incorporating extra copper ions to the chemically defined medium (CDM) complemented the function of <i>cbiO</i> for biofilm formation in a dose-dependent manner, while the addition of extra iron ions in CDM enhanced the effect of <i>cbiO</i> null mutation on biofilm formation. In addition, neither the addition of certain extra amounts of copper ions nor iron ions in CDM had an impact on bacterial growth. Taken together, our findings suggest that <i>cbiO</i> mediates biofilm formation by affecting the transportation of copper ions in the MRSA CFSa36 strain. This study provides new insights into the molecular basis of biofilm formation by <i>S. aureus</i>.
format article
author Ying Liu
Junshu Yang
Michelle Ji
James Phillips
Mark Wylam
Yinduo Ji
author_facet Ying Liu
Junshu Yang
Michelle Ji
James Phillips
Mark Wylam
Yinduo Ji
author_sort Ying Liu
title Identification of <i>cbiO</i> Gene Critical for Biofilm Formation by MRSA CFSa36 Strain Isolated from Pediatric Patient with Cystic Fibrosis
title_short Identification of <i>cbiO</i> Gene Critical for Biofilm Formation by MRSA CFSa36 Strain Isolated from Pediatric Patient with Cystic Fibrosis
title_full Identification of <i>cbiO</i> Gene Critical for Biofilm Formation by MRSA CFSa36 Strain Isolated from Pediatric Patient with Cystic Fibrosis
title_fullStr Identification of <i>cbiO</i> Gene Critical for Biofilm Formation by MRSA CFSa36 Strain Isolated from Pediatric Patient with Cystic Fibrosis
title_full_unstemmed Identification of <i>cbiO</i> Gene Critical for Biofilm Formation by MRSA CFSa36 Strain Isolated from Pediatric Patient with Cystic Fibrosis
title_sort identification of <i>cbio</i> gene critical for biofilm formation by mrsa cfsa36 strain isolated from pediatric patient with cystic fibrosis
publisher MDPI AG
publishDate 2021
url https://doaj.org/article/5739aaa053d140b2b5a4a2087df98037
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