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IL-8 and global gene expression analysis define a key role of ATP in renal epithelial cell responses induced by uropathogenic bacteria
Örebro University, School of Medicine, Örebro University, Sweden. Örebro University Hospital. iRiSC — Inflammatory Response and Infection Susceptibility Centre, Faculty of Medicine and Health, Örebro University, Örebro, Sweden; Clinical Research Centre (KFC), Örebro University Hospital, Örebro, Sweden.
Örebro University, School of Health and Medical Sciences, Örebro University, Sweden.
School of Natural Sciences, Linnaeus University, Kalmar, Sweden.
Örebro University, School of Medicine, Örebro University, Sweden. iRiSC — Inflammatory Response and Infection Susceptibility Centre, Faculty of Medicine and Health, Örebro University, Örebro, Sweden.
2014 (English)In: Purinergic Signalling Purinergic Signalling, ISSN 1573-9538, E-ISSN 1573-9546, Vol. 10, no 3, 499-508 p.Article in journal (Refereed) Published
Abstract [en]

The recent recognition of receptor-mediated ATP signalling as a pathway of epithelial pro-inflammatory cytokine release challenges the ubiquitous role of the TLR4 pathway during urinary tract infection. The aim of this study was to compare cellular responses of renal epithelial cells infected with uropathogenic Escherichia coli (UPEC) strain IA2 to stimulation with ATP-gamma-S. A498 cells were infected or stimulated in the presence or absence of apyrase, that degrades extracellular ATP, or after siRNA-mediated knockdown of ATP-responding P2Y(2) receptors. Cellular IL-8 release and global gene expression were analysed. Both IA2 and A498 cells per se released ATP, which increased during infection. IA2 and ATP-gamma-S caused a similar to 5-fold increase in cellular release of IL-8 and stimulations performed in the presence of apyrase or after siRNA knockdown of P2Y(2) receptors resulted in attenuation of IA2-mediated IL-8 release. Microarray results show that both IA2 and ATP-gamma-S induced marked changes in gene expression of renal cells. Thirty-six genes were in common between both stimuli, and many of these are key genes belonging to classical response pathways of bacterial infection. Functional analysis shows that 88 biological function-annotated cellular pathways were identical between IA2 and ATP-gamma-S stimuli. Results show that UPEC-induced release of IL-8 is dependent on P2Y(2) signalling and that cellular responses elicited by UPEC and ATP-gamma-S have many identical features. This indicates that renal epithelial responses elicited by bacteria could be mediated by bacteria- or host-derived ATP, thus defining a key role of ATP during infection.

Place, publisher, year, edition, pages
Dordrect, Netherlands: Springer, 2014. Vol. 10, no 3, 499-508 p.
Keyword [en]
Urinary tract infection, Host response, Adenosine triphosphate, Uropathogenic E. coli, Purinergic P2Y receptors
National Category
Neurology
Research subject
Neurology; Molecular Biology
Identifiers
URN: urn:nbn:se:oru:diva-37678DOI: 10.1007/s11302-014-9414-7ISI: 000341772500009PubMedID: 24817659Scopus ID: 2-s2.0-84930902388OAI: oai:DiVA.org:oru-37678DiVA: diva2:754860
Note

Funding Agencies:

Magnus Bergvalls Foundation

Faculty of Medicine and Health at Orebro University

Available from: 2014-10-13 Created: 2014-10-13 Last updated: 2017-10-18Bibliographically approved

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Kruse, RobertDemirel, IsakPersson, Katarina
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School of Medicine, Örebro University, SwedenÖrebro University HospitalSchool of Health and Medical Sciences, Örebro University, Sweden
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Purinergic Signalling Purinergic Signalling
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