Proteomic Adaptation of Australian Epidemic Bordetella pertussis.
- Publisher:
- Wiley
- Publication Type:
- Journal Article
- Citation:
- Proteomics, 2018, 18, (8), pp. 1-12
- Issue Date:
- 2018-04
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| Filename | Description | Size | |||
|---|---|---|---|---|---|
| Proteomics - 2018 - Luu - Proteomic Adaptation of Australian Epidemic Bordetella pertussis.pdf | Published version | 800.94 kB |
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Full metadata record
| Field | Value | Language |
|---|---|---|
| dc.contributor.author | Luu, LDW | |
| dc.contributor.author | Octavia, S | |
| dc.contributor.author | Zhong, L | |
| dc.contributor.author | Raftery, MJ | |
| dc.contributor.author | Sintchenko, V | |
| dc.contributor.author | Lan, R | |
| dc.date.accessioned | 2022-09-05T07:39:42Z | |
| dc.date.available | 2022-09-05T07:39:42Z | |
| dc.date.issued | 2018-04 | |
| dc.identifier.citation | Proteomics, 2018, 18, (8), pp. 1-12 | |
| dc.identifier.issn | 1615-9853 | |
| dc.identifier.issn | 1615-9861 | |
| dc.identifier.uri | http://hdl.handle.net/10453/161370 | |
| dc.description.abstract | Bordetella pertussis causes whooping cough. The predominant strains in Australia changed to single nucleotide polymorphism (SNP) cluster I (pertussis toxin promoter allele ptxP3/pertactin gene allele prn2) from cluster II (non-ptxP3/non-prn2). Cluster I was mostly responsible for the 2008-2012 Australian epidemic and was found to have higher fitness compared to cluster II using an in vivo mouse competition assay, regardless of host's immunization status. This study aimed to identify proteomic differences that explain higher fitness in cluster I using isobaric tags for relative and absolute quantification (iTRAQ), and high-resolution multiple reaction monitoring (MRM-hr). A few key differences in the whole cell and secretome were identified between the cluster I and II strains tested. In the whole cell, nine proteins were upregulated (>1.2 fold change, q < 0.05) and three were downregulated (<0.8 fold change, q < 0.05) in cluster I. One downregulated protein was BP1569, a TLR2 agonist for Th1 immunity. In the secretome, 12 proteins were upregulated and 1 was downregulated which was Bsp22, a type III secretion system (T3SS) protein. Furthermore, there was a trend of downregulation in three T3SS effectors and other virulence factors. Three proteins were upregulated in both whole cell and supernatant: BP0200, molybdate ABC transporter (ModB), and tracheal colonization factor A (TcfA). Important expression differences in lipoprotein, T3SS, and transport proteins between the cluster I and II strains were identified. These differences may affect immune evasion, virulence and metabolism, and play a role in increased fitness of cluster I. | |
| dc.format | ||
| dc.language | eng | |
| dc.publisher | Wiley | |
| dc.relation.ispartof | Proteomics | |
| dc.relation.isbasedon | 10.1002/pmic.201700237 | |
| dc.rights | info:eu-repo/semantics/closedAccess | |
| dc.subject | 06 Biological Sciences, 08 Information and Computing Sciences, 11 Medical and Health Sciences | |
| dc.subject.classification | Biochemistry & Molecular Biology | |
| dc.subject.mesh | Australia | |
| dc.subject.mesh | Bacterial Outer Membrane Proteins | |
| dc.subject.mesh | Bacterial Proteins | |
| dc.subject.mesh | Bordetella pertussis | |
| dc.subject.mesh | Gene Expression Regulation, Bacterial | |
| dc.subject.mesh | Humans | |
| dc.subject.mesh | Pertussis Toxin | |
| dc.subject.mesh | Polymorphism, Single Nucleotide | |
| dc.subject.mesh | Proteomics | |
| dc.subject.mesh | Type III Secretion Systems | |
| dc.subject.mesh | Virulence Factors, Bordetella | |
| dc.subject.mesh | Whooping Cough | |
| dc.subject.mesh | Australia | |
| dc.subject.mesh | Bacterial Outer Membrane Proteins | |
| dc.subject.mesh | Bacterial Proteins | |
| dc.subject.mesh | Bordetella pertussis | |
| dc.subject.mesh | Gene Expression Regulation, Bacterial | |
| dc.subject.mesh | Humans | |
| dc.subject.mesh | Pertussis Toxin | |
| dc.subject.mesh | Polymorphism, Single Nucleotide | |
| dc.subject.mesh | Proteomics | |
| dc.subject.mesh | Type III Secretion Systems | |
| dc.subject.mesh | Virulence Factors, Bordetella | |
| dc.subject.mesh | Whooping Cough | |
| dc.subject.mesh | Humans | |
| dc.subject.mesh | Bordetella pertussis | |
| dc.subject.mesh | Whooping Cough | |
| dc.subject.mesh | Pertussis Toxin | |
| dc.subject.mesh | Bacterial Proteins | |
| dc.subject.mesh | Bacterial Outer Membrane Proteins | |
| dc.subject.mesh | Virulence Factors, Bordetella | |
| dc.subject.mesh | Proteomics | |
| dc.subject.mesh | Gene Expression Regulation, Bacterial | |
| dc.subject.mesh | Polymorphism, Single Nucleotide | |
| dc.subject.mesh | Australia | |
| dc.subject.mesh | Type III Secretion Systems | |
| dc.title | Proteomic Adaptation of Australian Epidemic Bordetella pertussis. | |
| dc.type | Journal Article | |
| utslib.citation.volume | 18 | |
| utslib.location.activity | Germany | |
| utslib.for | 06 Biological Sciences | |
| utslib.for | 08 Information and Computing Sciences | |
| utslib.for | 11 Medical and Health Sciences | |
| pubs.organisational-group | /University of Technology Sydney | |
| pubs.organisational-group | /University of Technology Sydney/Faculty of Science | |
| pubs.organisational-group | /University of Technology Sydney/Faculty of Science/School of Life Sciences | |
| utslib.copyright.status | closed_access | * |
| pubs.consider-herdc | false | |
| dc.date.updated | 2022-09-05T07:39:41Z | |
| pubs.issue | 8 | |
| pubs.publication-status | Published | |
| pubs.volume | 18 | |
| utslib.citation.issue | 8 |
Abstract:
Bordetella pertussis causes whooping cough. The predominant strains in Australia changed to single nucleotide polymorphism (SNP) cluster I (pertussis toxin promoter allele ptxP3/pertactin gene allele prn2) from cluster II (non-ptxP3/non-prn2). Cluster I was mostly responsible for the 2008-2012 Australian epidemic and was found to have higher fitness compared to cluster II using an in vivo mouse competition assay, regardless of host's immunization status. This study aimed to identify proteomic differences that explain higher fitness in cluster I using isobaric tags for relative and absolute quantification (iTRAQ), and high-resolution multiple reaction monitoring (MRM-hr). A few key differences in the whole cell and secretome were identified between the cluster I and II strains tested. In the whole cell, nine proteins were upregulated (>1.2 fold change, q < 0.05) and three were downregulated (<0.8 fold change, q < 0.05) in cluster I. One downregulated protein was BP1569, a TLR2 agonist for Th1 immunity. In the secretome, 12 proteins were upregulated and 1 was downregulated which was Bsp22, a type III secretion system (T3SS) protein. Furthermore, there was a trend of downregulation in three T3SS effectors and other virulence factors. Three proteins were upregulated in both whole cell and supernatant: BP0200, molybdate ABC transporter (ModB), and tracheal colonization factor A (TcfA). Important expression differences in lipoprotein, T3SS, and transport proteins between the cluster I and II strains were identified. These differences may affect immune evasion, virulence and metabolism, and play a role in increased fitness of cluster I.
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