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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
Univ Örebro.
Univ Örebro.
Linnaeus University, Faculty of Health and Life Sciences, Department of Chemistry and Biomedical Sciences.
Univ Örebro.
2014 (English)In: Purinergic Signalling Purinergic Signalling, ISSN 1573-9538, 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
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
Medical Biotechnology (with a focus on Cell Biology (including Stem Cell Biology), Molecular Biology, Microbiology, Biochemistry or Biopharmacy)
Research subject
Natural Science, Biomedical Sciences
Identifiers
URN: urn:nbn:se:lnu:diva-37856DOI: 10.1007/s11302-014-9414-7ISI: 000341772500009OAI: oai:DiVA.org:lnu-37856DiVA: diva2:758209
Available from: 2014-10-24 Created: 2014-10-24 Last updated: 2014-10-24Bibliographically approved

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Säve, Susanne
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Purinergic Signalling Purinergic Signalling
Medical Biotechnology (with a focus on Cell Biology (including Stem Cell Biology), Molecular Biology, Microbiology, Biochemistry or Biopharmacy)

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CiteExportLink to record
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Citation style
  • apa
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More styles
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