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Transcriptional profiling of human macrophages during infection with Bordetella pertussis
D. Petráčková, MR. Farman, F. Amman, I. Linhartová, A. Dienstbier, D. Kumar, J. Držmíšek, I. Hofacker, ME. Rodriguez, B. Večerek
Language English Country United States
Document type Journal Article, Research Support, Non-U.S. Gov't
Grant support
NV16-30782A
MZ0
CEP Register
Digital library NLK
Full text - Article
NLK
Free Medical Journals
from 2004 to 1 year ago
Freely Accessible Science Journals
from 2004
PubMed Central
from 2009 to 1 year ago
Europe PubMed Central
from 2009 to 1 year ago
- MeSH
- Bordetella pertussis physiology MeSH
- Cell Line MeSH
- Gene Ontology MeSH
- Gene Regulatory Networks MeSH
- Host-Pathogen Interactions genetics immunology MeSH
- Cells, Cultured MeSH
- Real-Time Polymerase Chain Reaction MeSH
- Humans MeSH
- Macrophages immunology metabolism microbiology MeSH
- Whooping Cough genetics immunology virology MeSH
- Gene Expression Regulation MeSH
- Reproducibility of Results MeSH
- Gene Expression Profiling * methods MeSH
- Transcriptome * MeSH
- Computational Biology methods MeSH
- Check Tag
- Humans MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
Bordetella pertussis, a strictly human re-emerging pathogen and the causative agent of whooping cough, exploits a broad variety of virulence factors to establish efficient infection. Here, we used RNA sequencing to analyse the changes in gene expression profiles of human THP-1 macrophages resulting from B. pertussis infection. In parallel, we attempted to determine the changes in intracellular B. pertussis-specific transcriptomic profiles resulting from interaction with macrophages. Our analysis revealed that global gene expression profiles in THP-1 macrophages are extensively rewired 6 h post-infection. Among the highly expressed genes, we identified those encoding cytokines, chemokines, and transcription regulators involved in the induction of the M1 and M2 macrophage polarization programmes. Notably, several host genes involved in the control of apoptosis and inflammation which are known to be hijacked by intracellular bacterial pathogens were overexpressed upon infection. Furthermore, in silico analyses identified large temporal changes in expression of specific gene subsets involved in signalling and metabolic pathways. Despite limited numbers of the bacterial reads, we observed reduced expression of majority of virulence factors and upregulation of several transcriptional regulators during infection suggesting that intracellular B. pertussis cells switch from virulent to avirulent phase and actively adapt to intracellular environment, respectively.
Division of Cell and Developmental Biology Medical University of Vienna Vienna Austria
Facultad de Ciencias Exactas Universidad Nacional de La Plata CINDEFI La Plata Argentina
Institute for Theoretical Chemistry University of Vienna Vienna Austria
References provided by Crossref.org
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