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Co-transcriptomes of initial interactions in vitro between streptococcus Pneumoniae and human pleural mesothelial cells

Co-transcriptomes of initial interactions in vitro between streptococcus Pneumoniae and human pleural mesothelial cells
Co-transcriptomes of initial interactions in vitro between streptococcus Pneumoniae and human pleural mesothelial cells
Streptococcus pneumoniae (Spn) is a major causative organism of empyema, an inflammatory condition occurring in the pleural sac. In this study, we used human and Spn cDNA microarrays to characterize the transcriptional responses occurring during initial contact between Spn and a human pleural mesothelial cell line (PMC) in vitro. Using stringent filtering criteria, 42 and 23 Spn genes were up-and down-regulated respectively. In particular, genes encoding factors potentially involved in metabolic processes and Spn adherence to eukaryotic cells were up-regulated e.g. glnQ, glnA, aliA, psaB, lytB and nox. After Spn initial contact, 870 human genes were differentially regulated and the largest numbers of significant gene expression changes were found in canonical pathways for eukaryotic initiation factor 2 signaling (60 genes out of 171), oxidative phosphorylation (32/103), mitochondrial dysfunction (37/164), eIF4 and p70S6K signaling (28/142), mTOR signaling (27/182), NRF2-mediated oxidative stress response (20/177), epithelial adherens junction remodeling (11/66) and ubiquitination (22/254). The cellular response appeared to be directed towards host cell survival and defense. Spn did not activate NF-kB or phosphorylate p38 MAPK or induce cytokine production from PMC. Moreover, Spn infection of TNF-? pre-stimulated PMC inhibited production of IL-6 and IL-8 secretion by >50% (p<0.01). In summary, this descriptive study provides datasets and a platform for examining further the molecular mechanisms underlying the pathogenesis of empyema
1932-6203
e0142773-[26pp]
Heath, Claire Jane
dc0c868c-6448-47a8-ae09-ae09991d5ad3
Cendra, Maria del Mar
150d34a4-4598-4138-96c0-06f3f338cca2
Watson, Alastair
9eb79329-8d32-4ed4-b8b9-d720883e8042
Auger, Jean-Phillipe
3840cda6-6366-47b9-a5b6-42100986a5a3
Pandey, Anish
0be0525d-d74b-46ab-961d-611fd0dd759e
Tighe, Paddy
a97aafd0-1fa3-4426-8c4b-c940b379d71a
Christodoulides, Myron
eba99148-620c-452a-a334-c1a52ba94078
Heath, Claire Jane
dc0c868c-6448-47a8-ae09-ae09991d5ad3
Cendra, Maria del Mar
150d34a4-4598-4138-96c0-06f3f338cca2
Watson, Alastair
9eb79329-8d32-4ed4-b8b9-d720883e8042
Auger, Jean-Phillipe
3840cda6-6366-47b9-a5b6-42100986a5a3
Pandey, Anish
0be0525d-d74b-46ab-961d-611fd0dd759e
Tighe, Paddy
a97aafd0-1fa3-4426-8c4b-c940b379d71a
Christodoulides, Myron
eba99148-620c-452a-a334-c1a52ba94078

Heath, Claire Jane, Cendra, Maria del Mar, Watson, Alastair, Auger, Jean-Phillipe, Pandey, Anish, Tighe, Paddy and Christodoulides, Myron (2015) Co-transcriptomes of initial interactions in vitro between streptococcus Pneumoniae and human pleural mesothelial cells. PLoS ONE, 10 (11), e0142773-[26pp]. (doi:10.1371/journal.pone.0142773). (PMID:26566142)

Record type: Article

Abstract

Streptococcus pneumoniae (Spn) is a major causative organism of empyema, an inflammatory condition occurring in the pleural sac. In this study, we used human and Spn cDNA microarrays to characterize the transcriptional responses occurring during initial contact between Spn and a human pleural mesothelial cell line (PMC) in vitro. Using stringent filtering criteria, 42 and 23 Spn genes were up-and down-regulated respectively. In particular, genes encoding factors potentially involved in metabolic processes and Spn adherence to eukaryotic cells were up-regulated e.g. glnQ, glnA, aliA, psaB, lytB and nox. After Spn initial contact, 870 human genes were differentially regulated and the largest numbers of significant gene expression changes were found in canonical pathways for eukaryotic initiation factor 2 signaling (60 genes out of 171), oxidative phosphorylation (32/103), mitochondrial dysfunction (37/164), eIF4 and p70S6K signaling (28/142), mTOR signaling (27/182), NRF2-mediated oxidative stress response (20/177), epithelial adherens junction remodeling (11/66) and ubiquitination (22/254). The cellular response appeared to be directed towards host cell survival and defense. Spn did not activate NF-kB or phosphorylate p38 MAPK or induce cytokine production from PMC. Moreover, Spn infection of TNF-? pre-stimulated PMC inhibited production of IL-6 and IL-8 secretion by >50% (p<0.01). In summary, this descriptive study provides datasets and a platform for examining further the molecular mechanisms underlying the pathogenesis of empyema

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Accepted/In Press date: 27 October 2015
Published date: 13 November 2015
Organisations: Clinical & Experimental Sciences

Identifiers

Local EPrints ID: 384041
URI: https://eprints.soton.ac.uk/id/eprint/384041
ISSN: 1932-6203
PURE UUID: 950b436b-b324-412a-980d-ff82f3cbf0d7

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Date deposited: 08 Dec 2015 13:04
Last modified: 13 Jun 2018 16:31

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Contributors

Author: Claire Jane Heath
Author: Maria del Mar Cendra
Author: Alastair Watson
Author: Jean-Phillipe Auger
Author: Anish Pandey
Author: Paddy Tighe

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