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Persson, Katarina
Publications (10 of 77) Show all publications
Demirel, I., Säve, S., Kruse, R. & Persson, K. (2013). Expression of suppressor of cytokine signalling 3 (SOCS3) in human bladder epithelial cells infected with uropathogenic Escherichia coli. Acta Pathologica, Microbiologica et Immunologica Scandinavica (APMIS), 121(2), 158-167
Open this publication in new window or tab >>Expression of suppressor of cytokine signalling 3 (SOCS3) in human bladder epithelial cells infected with uropathogenic Escherichia coli
2013 (English)In: Acta Pathologica, Microbiologica et Immunologica Scandinavica (APMIS), ISSN 0903-4641, E-ISSN 1600-0463, Vol. 121, no 2, p. 158-167Article in journal (Refereed) Published
Abstract [en]

Suppressor of cytokine signalling (SOCS) proteins inhibit pro-inflammatory signalling mediated by Janus-activated kinase (JAK)-signal transducer and activator of transcription (STAT) pathways. To evade the immune response some pathogens appear to modify the host SOCS proteins. Uropathogenic Escherichia coli (UPEC) are able to subvert the host response evoked by bladder epithelial cells, but the mechanisms are not fully understood. The objective of this study was to investigate whether UPEC can modify the host SOCS and STAT3 response. Real time RT-PCR studies demonstrated an increased SOCS1 and SOCS3 expression in the isolated human bladder epithelial cell lines (RT-4 and 5637) in response to cytokines. UPEC strain IA2 increased SOCS3, but not SOCS1, mRNA levels with a peak at 6h after infection. The increase of SOCS3 was confirmed at the protein level by Western blotting. The UPEC strain IA2 caused a time-dependent decrease in the phosphorylation of STAT3. This study demonstrates that UPEC are able to affect SOCS3 and STAT3 signalling in human uroepithelial cells. The finding that UPEC are able to induce mediators involved in suppression of host cytokine signalling may help to elucidate how UPEC may circumvent the host response during urinary tract infection.

Keywords
Bladder epithelial cells, uropathogenic Escherichia coli, host response, signal transducer and activator of transcription 3, suppressor of cytokine signalling
National Category
Microbiology in the medical area Cell and Molecular Biology Urology and Nephrology
Research subject
Natural Science, Biomedical Sciences
Identifiers
urn:nbn:se:lnu:diva-24532 (URN)10.1111/j.1600-0463.2012.02951.x (DOI)000313830700010 ()2-s2.0-84872654631 (Scopus ID)
Available from: 2013-02-25 Created: 2013-02-25 Last updated: 2018-01-11Bibliographically approved
Kruse, R., Säve, S. & Persson, K. (2012). Adenosine Triphosphate Induced P2Y(2) Receptor Activation Induces Proinflammatory Cytokine Release in Uroepithelial Cells.. Journal of Urology, 188(6), 2419-2425
Open this publication in new window or tab >>Adenosine Triphosphate Induced P2Y(2) Receptor Activation Induces Proinflammatory Cytokine Release in Uroepithelial Cells.
2012 (English)In: Journal of Urology, ISSN 0022-5347, E-ISSN 1527-3792, Vol. 188, no 6, p. 2419-2425Article in journal (Refereed) Published
Abstract [en]

PURPOSE: We characterized and identified the uroepithelial P2 receptor responsible for adenosine triphosphate mediated release of the cytokines interleukin-8 and 6.

MATERIALS AND METHODS: The human renal epithelial cell line A498 (ATCC™) was cultured and stimulated with different purinergic agonists with or without prior inhibition with different antagonists or signaling pathway inhibitors. Supernatant was analyzed for interleukin-8 and 6 by enzyme-linked immunosorbent assay. P2 receptor mRNA expression was assessed by real-time reverse transcriptase-polymerase chain reaction. The candidate receptor was knocked down with siRNA technology. Interleukin-8 and 6 responses were measured after purinergic stimulation of knocked down cells.

RESULTS: ATP and ATP-γ-S (Roche Diagnostics, Mannheim, Germany) were equipotent as inducers of interleukin-8 and 6 release. Agonist profile experiments using different P2 receptor agonists indicated that P2Y(2) was the main contributor to this release, although P2Y(11) and P2X(7) activation could not be excluded. Signaling pathway experiments showed that interleukin-8 release involved phospholipase C and inositol trisphosphate mediated signaling, indicating a P2Y receptor subtype. Antagonist experiments indicated P2Y(2) as the responsible receptor. Gene expression analysis of P2 receptors showed that strong expression of P2Y(2) receptor and subsequent knockdown of P2Y(2) receptor mRNA for 72 and 96 hours abrogated interleukin-8 and 6 release after purinergic stimulation with adenosine triphosphate-γ-S.

CONCLUSIONS: Interleukin-8 and 6 release after purinergic stimulation in uroepithelial A498 cells is mediated through P2Y(2) receptor activation.

National Category
Urology and Nephrology Immunology in the medical area
Research subject
Natural Science, Biomedical Sciences
Identifiers
urn:nbn:se:lnu:diva-22804 (URN)10.1016/j.juro.2012.07.095 (DOI)23088987 (PubMedID)2-s2.0-84869079425 (Scopus ID)
Available from: 2012-12-12 Created: 2012-12-12 Last updated: 2018-01-12Bibliographically approved
Demirel, I., Vumma, R., Mohlin, C., Svensson, L., Säve, S. & Persson, K. (2012). Nitric Oxide Activates IL-6 Production and Expression in Human Renal Epithelial Cells. American Journal of Nephrology, 36(6), 524-530
Open this publication in new window or tab >>Nitric Oxide Activates IL-6 Production and Expression in Human Renal Epithelial Cells
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2012 (English)In: American Journal of Nephrology, ISSN 0250-8095, E-ISSN 1421-9670, Vol. 36, no 6, p. 524-530Article in journal (Refereed) Published
Abstract [en]

Background/Aims: Increased nitric oxide (NO) production or inducible form of NO synthase activity have been documented in patients suffering from urinary tract infection (UTI), but the role of NO in this infection is unclear. We investigated whether NO can affect the host response in human renal epithelial cells by modulating IL-6 production and mRNA expression. Methods: The human renal epithelial cell line A498 was infected with a uropathogenic Escherichia coli (UPEC) strain and/or the NO donor DETA/NO. The IL-6 production and mRNA expression were evaluated by ELISA and real-time RT-PCR. IL-6 mRNA stability was evaluated by analyzing mRNA degradation by real-time RT-PCR. Results: DETA/NO caused a significant (p < 0.05) increase in IL-6 production. Inhibitors of p38 MAPK and ERK1/2 signaling, but not JNK, were shown to significantly suppress DETA/NO-induced IL-6 production. UPEC-induced IL-6 production was further increased (by 73 +/- 23%, p < 0.05) in the presence of DETA/NO. The IL-6 mRNA expression increased 2.1 +/- 0.17-fold in response to DETA/NO, while the UPEC-evoked increase was pronounced (20 +/- 4.5-fold). A synergistic effect of DETA/NO on UPEC-induced IL-6 expression was found (33 +/- 7.2-fold increase). The IL-6 mRNA stability studies showed that DETA/NO partially attenuated UPEC-induced degradation of IL-6 mRNA. Conclusions: NO was found to stimulate IL-6 in renal epithelial cells through p38 MAPK and ERK1/2 signaling pathways and also to increase IL-6 mRNA stability in UPEC-infected cells. This study proposes a new role for NO in the host response during UTI by modulating the transcription and production of the cytokine IL-6. Copyright (C) 2012 S. Karger AG, Basel

Keywords
Nitric oxide, Urinary tract infections, IL-6, MAPK signaling, Renal epithelial cells
National Category
Urology and Nephrology Immunology in the medical area
Research subject
Natural Science, Biomedical Sciences
Identifiers
urn:nbn:se:lnu:diva-24513 (URN)10.1159/000345351 (DOI)000312916200004 ()2-s2.0-84869889861 (Scopus ID)
Available from: 2013-02-22 Created: 2013-02-22 Last updated: 2018-01-11Bibliographically approved
Säve, S., Mohlin, C., Vumma, R. & Persson, K. (2011). Activation of Adenosine A(2A) Receptors Inhibits Neutrophil Transuroepithelial Migration. Infection and Immunity, 79(8), 3431-3437
Open this publication in new window or tab >>Activation of Adenosine A(2A) Receptors Inhibits Neutrophil Transuroepithelial Migration
2011 (English)In: Infection and Immunity, ISSN 0019-9567, E-ISSN 1098-5522, Vol. 79, no 8, p. 3431-3437Article in journal (Refereed) Published
Abstract [en]

Adenosine has been identified as a significant inhibitor of inflammation by acting on adenosine A(2A) receptors. In this study, we examined the role of adenosine and A(2A) receptors in the transmigration of human neutrophils across an in vitro model of the transitional bladder urothelium. Human uroepithelial cells (UROtsa) were grown on transwell inserts; uropathogenic Escherichia coli (UPEC) and neutrophils were added to the transwell system; and the number of migrating neutrophils was evaluated. Reverse transcription-PCR (RT-PCR), immunohistochemistry, and flow cytometry were used to investigate the expression of adenosine receptors, the epithelial adhesion molecule ICAM-1, and the neutrophil integrin CD11b. Levels of proinflammatory interleukin-8 (IL-8) and phosphorylated I kappa B alpha were measured by enzyme-linked immunosorbent assays (ELISA) and Luminex assays, respectively. The neutrophils expressed all four adenosine receptor subtypes (A(1), A(2A), A(2B), and A(3) receptors), but A(3) receptors were not expressed by UROtsa cells. UPEC stimulated neutrophil transuroepithelial migration, which was significantly decreased in response to the specific A(2A) receptor agonist CGS 21680. The inhibitory effect of CGS 21680 on neutrophil migration was reversed by the A(2A) receptor antagonist SCH 58261. The production of chemotactic IL-8 and the expression of the adhesion molecule ICAM-1 or CD11b were not significantly affected by CGS 21680. However, a significant decrease in the level of phosporylated I kappa B alpha was revealed in response to CGS 21680. In conclusion, UPEC infection in vitro evoked neutrophil migration through a multilayered human uroepithelium. The UPEC-evoked neutrophil transmigration decreased in response to A(2A) receptor activation, possibly through inhibition of NF-kappa B signaling pathways.

National Category
Medical and Health Sciences
Research subject
Natural Science, Biomedical Sciences
Identifiers
urn:nbn:se:lnu:diva-16180 (URN)10.1128/IAI.05005-11 (DOI)000292770300047 ()2-s2.0-79961106306 (Scopus ID)
Available from: 2011-12-16 Created: 2011-12-16 Last updated: 2017-12-08Bibliographically approved
Säve, S. & Persson, K. (2010). Effects of Adenosine A(2A) and A(2B) Receptor Activation on Signaling Pathways and Cytokine Production in Human Uroepithelial Cells. Pharmacology, 86(3), 129-137
Open this publication in new window or tab >>Effects of Adenosine A(2A) and A(2B) Receptor Activation on Signaling Pathways and Cytokine Production in Human Uroepithelial Cells
2010 (English)In: Pharmacology, ISSN 0031-7012, E-ISSN 1423-0313, Vol. 86, no 3, p. 129-137Article in journal (Refereed) Published
Abstract [en]

Aims: Adenosine A(2A) and A(2B) receptor subtypes have both been implicated in the modulation of inflammation. We examined adenosine A(2A) and A(2B) receptor expression, signaling pathways and the effect of adenosine A(2A) and A(2B) receptor activation on the uropathogenic Escherichia coli (UPEC)-stimulated IL-8 response in human uroepithelial cells (UROtsa). Methods: Receptor expression was examined by RT-PCR and Western blot, and IL-8 production, intracellular cAMP levels and phosphoproteins were measured by ELISA, EIA and multiplex immunoassay, respectively. Results: The adenosine A(1), A(2A) and A(2B) receptor subtypes were detected in UROtsa cells. The adenosine A(2A) receptor agonist CGS 21680 did not stimulate cAMP production but CREB phosphorylation was slightly increased. The adenosine A(2) receptor agonist CPCA induced a pronounced cAMP and CREB response. Furthermore, CGS 21680 but not CPCA decreased ERK 1/2 and STAT3 phosphorylation. UPEC infection stimulated the host IL-8 production but CPCA or CGS 21680 did not affect UPEC-evoked IL-8 production. Conclusions: Our data identified differences in signaling pathways evoked by adenosine A(2A) and A(2B) receptor activation. Activation of the adenosine A(2A) receptor inhibited STAT3 and ERK 1/2 phosphorylation, while the cAMP-CREB pathway was induced by adenosine A(2B) receptor activation. No anti-or proinflammatory effects were found for uroepithelial adenosine A(2A) or A(2B) receptors. Copyright (C) 2010 S. Karger AG, Basel

Keywords
Adenosine receptors, Cyclic AMP, Interleukin-8, Urinary tract infection, Uropathogenic Escherichia coli
National Category
Medical and Health Sciences
Research subject
Natural Science, Biomedical Sciences
Identifiers
urn:nbn:se:lnu:diva-16182 (URN)10.1159/000317068 (DOI)000281224500001 ()2-s2.0-77955110191 (Scopus ID)
Available from: 2011-12-16 Created: 2011-12-16 Last updated: 2017-12-08Bibliographically approved
Säve, S. & Persson, K. (2010). Extracellular ATP and P2Y Receptor Activation Induce a Proinflammatory Host Response in the Human Urinary Tract. Infection and Immunity, 78(8), 3609-3615
Open this publication in new window or tab >>Extracellular ATP and P2Y Receptor Activation Induce a Proinflammatory Host Response in the Human Urinary Tract
2010 (English)In: Infection and Immunity, ISSN 0019-9567, E-ISSN 1098-5522, Vol. 78, no 8, p. 3609-3615Article in journal (Refereed) Published
Abstract [en]

Extracellular ATP can be released by many cell types under conditions of cellular stress and signals through activation of purinergic receptors. Bladder uroepithelial cells grown in vitro have previously been shown to release ATP in response to stretch. In the present study, we investigated ATP release from uroepithelial cells infected with bacteria and the effect of ATP on the host cell proinflammatory interleukin 8 (IL-8) response. The human kidney epithelial cell line A498 and the human uroepithelial cell line UROtsa were grown in culture and stimulated by the uropathogenic Escherichia coli (UPEC) IA2 strain or the stable ATP analogue ATP-gamma-S. ATP and IL-8 levels were measured in cell culture medium with a luciferin-luciferase assay and enzyme-linked immunosorbent assay (ELISA), respectively. The results showed that UPEC infection of uroepithelial cells for 1 h significantly increased (P < 0.01) the extracellular ATP levels. ATP-gamma-S (10 and 100 mu M) stimulated release of IL-8 from UROtsa and A498 cells after 6 and 24 h. Experiments with different purinoceptor agonists suggested that P2Y receptors, and not P2X receptors, were responsible for the ATP-gamma-S-induced IL-8 release. The potency profile further suggested involvement of P2Y(1), P2Y(2), and/or P2Y(11) receptors, and reverse transcription-PCR (RT-PCR) studies confirmed that the cells expressed these receptors. The amount of IL-8 released increased 12-fold in UPEC-infected cells, and apyrase, an enzyme that degrades ATP, reduced this increase by approximately 50%. The present study suggests that enhanced ATP release and P2Y receptor activation during urinary tract infection may represent a novel, non-TLR4-mediated mechanism for production of proinflammatory IL-8 in human urinary tract epithelial cells.

National Category
Medical and Health Sciences
Research subject
Natural Science, Biomedical Sciences
Identifiers
urn:nbn:se:lnu:diva-16181 (URN)10.1128/IAI.00074-10 (DOI)000279990400029 ()2-s2.0-77955298675 (Scopus ID)
Available from: 2011-12-16 Created: 2011-12-16 Last updated: 2017-12-08Bibliographically approved
Svensson, L., Poljakovic, M., Säve, S., Gilberthorpe, N., Schön, T., Strid, S., . . . Persson, K. (2010). Role of flavohemoglobin in combating nitrosative stress in uropathogenic Escherichia coli – implications for urinary tract infection. Microbial Pathogenesis, 49(3), 59-66
Open this publication in new window or tab >>Role of flavohemoglobin in combating nitrosative stress in uropathogenic Escherichia coli – implications for urinary tract infection
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2010 (English)In: Microbial Pathogenesis, ISSN 0882-4010, E-ISSN 1096-1208, Vol. 49, no 3, p. 59-66Article in journal (Refereed) Published
Abstract [en]

During the course of urinary tract infection (UTI) nitric oxide (NO) is generated as part of the host response. This study investigates the significance of the NO-detoxifying enzyme flavohemoglobin (Hmp) in protection of uropathogenic Escherichia coli (UPEC) against nitrosative stress. An hmp (J96Δhmp) knockout mutant of UPEC strain J96 was constructed using single-gene deletion. The viability of J96Δhmp was significantly reduced (P < 0.001) compared to the wild-type strain after exposure to the NO-donor DETA/NO. The NO consumption in J96Δhmp was significantly (P < 0.001) impaired compared to J96wt. Screening UPEC isolates from patients with UTI revealed increased hmp expression in all patients. In a competition-based mouse model of UTI, the hmp mutant strain was significantly (P < 0.05) out-competed by the wild-type strain. This study demonstrates, for the first time, that Hmp contributes to the protection of UPEC against NO-mediated toxicity in vitro. In addition, hmp gene expression occurs in UPEC isolates from the infected human urinary tract and UPEC that were hmp-deficient had a reduced ability to colonize the mouse urinary tract. Taken together the results suggest that NO detoxification by Hmp may be a fitness advantage factor in UPEC, and a potentially interesting target for development of novel treatment concepts for UTI.

National Category
Microbiology in the medical area
Research subject
Natural Science, Biomedical Sciences
Identifiers
urn:nbn:se:lnu:diva-29102 (URN)10.1016/j.micpath.2010.04.001 (DOI)2-s2.0-77954660611 (Scopus ID)
Note

Ingår i avhandlingen "Nitric oxide and bacteria-host interactions in Escherichia coli urinary tract infection" under titeln "Flavohemoglobin protects uropathogenic Escherichia coli against nitrosative stress; implication for urovirulence"

Available from: 2013-09-30 Created: 2013-09-30 Last updated: 2018-10-24Bibliographically approved
Svensson, L., Säve, S. & Persson, K. (2010). The effect of nitric oxide on adherence of P-fimbriated uropathogenic Escherichia coli to human renal epithelial cells. British Journal of Urology, 105(12), 1726-1731
Open this publication in new window or tab >>The effect of nitric oxide on adherence of P-fimbriated uropathogenic Escherichia coli to human renal epithelial cells
2010 (English)In: British Journal of Urology, ISSN 0007-1331, E-ISSN 1365-2176, Vol. 105, no 12, p. 1726-1731Article in journal (Refereed) Published
Abstract [en]

OBJECTIVES

To examine the effect of nitric oxide (NO), an endogenous component of the host defence in urinary tract infection, on the adherence of P-fimbriated uropathogenic Escherichia coli (UPEC) to human renal epithelial cells.

MATERIALS AND METHODS

Two wild-type UPEC strains (AD110 and IA2) and the P-fimbriated recombinant strain HB101pPIL-75 were used. Bacteria were allowed to adhere to the human renal epithelial cell line A498 and attachment was evaluated in the absence or presence of the NO donor DETA/NONOate (1 mm). Total RNA was extracted from NO-exposed bacteria in static urine cultures, followed by semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR) analysis of the papG gene that encodes the P-fimbriae adhesin PapG.

RESULTS

Bacterial adherence to A498 cells was fimbriae-dependent and the ability to agglutinate human P1 positive erythrocytes confirmed that the used strains were P-fimbriated. UPEC strains AD110 and IA2 attached by a mean of 8 bacteria/cell and 20 bacteria/cell, respectively. In the presence of DETA/NONOate, the attachment of AD110 and IA2 to A498 cells was significantly reduced by a mean (sem) of 34 (3.9)% and 45 (14)%, respectively. The expression of papG was decreased after DETA/NONOate exposure as shown by semiquantitative RT-PCR.

CONCLUSION

NO disrupted functional adhesion of P-fimbriated UPEC to kidney epithelial cells, suggesting that NO-production from epithelial cells in the urinary tract may limit bacterial colonization at the mucosal surface. The reduced adherence may involve transcriptional effects of NO on papG expression, but further studies are needed to establish the underlying mechanisms.

National Category
Microbiology in the medical area
Research subject
Natural Science, Biomedical Sciences
Identifiers
urn:nbn:se:lnu:diva-29101 (URN)10.1111/j.1464-410X.2009.08986.x (DOI)
Available from: 2013-09-30 Created: 2013-09-30 Last updated: 2018-10-24Bibliographically approved
Säve, S., Mjösberg, J., Poljakovic, M., Mohlin, C. & Persson, K. (2009). Adenosine receptor expression in Escherichia coli-infected and cytokine-stimulated human urinary tract epithelial cells. BJU International, 104(11), 1758-1765
Open this publication in new window or tab >>Adenosine receptor expression in Escherichia coli-infected and cytokine-stimulated human urinary tract epithelial cells
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2009 (English)In: BJU International, ISSN 1464-4096, E-ISSN 1464-410X, Vol. 104, no 11, p. 1758-1765Article in journal (Refereed) Published
Abstract [en]

OBJECTIVETo assess the expression and regulation of adenosine receptors in unstimulated, uropathogenic Escherichia coli (UPEC)-infected and cytokine-stimulated human urinary tract epithelial cells, and to examine the regulation of interleukin (IL)-6 secretion in response to A(2A) receptor activation.

MATERIALS AND METHODSHuman urinary tract epithelial cells (A498, T24 and RT4) were grown in cell culture and stimulated with a mixture of pro-inflammatory cytokines (CM) or UPEC. The expression of adenosine receptors was evaluated using semiquantitative reverse transcription-polymerase chain reaction (RT-PCR), Western blot analysis and immunocytochemistry. IL-6 secretion was measured with an enzyme-linked immunosorbent assay.

RESULTSRT-PCR analysis showed the presence of transcripts for the A(1), A(2A) and A(2B) receptor subtypes but not for the A(3) receptor in A498 kidney epithelial cells. The expression of A(2A) receptor mRNA increased in A498 epithelial cells exposed to CM and UPEC, while A(1) and A(2B) receptor transcripts decreased or remained unchanged. Up-regulation of A(2A) receptors was confirmed at the protein level using Western blot analysis and immunocytochemistry. There was also an increase in A(2A) receptor mRNA in human bladder epithelial cells (T24 and RT4) and in mouse bladder uroepithelium in response to cytokines and UPEC. IL-6 secretion in UPEC-infected A498 cells was decreased by 38% when exposed to the A(2A) receptor agonist CGS 21680.

CONCLUSIONOur data showed a subtype-selective plasticity among adenosine receptors in urinary tract epithelial cells in response to UPEC-infection and cytokines. There was a consistent up-regulation of A(2A) receptors in kidney and bladder epithelial cells. Functionally, A(2A) receptor activation reduced UPEC-induced IL-6 secretion. These findings suggest that adenosine might be a previously unrecognized regulator of the mucosal response in urinary tract infection.

National Category
Medical and Health Sciences
Research subject
Biomedical Sciences, Pharmacology
Identifiers
urn:nbn:se:lnu:diva-2022 (URN)10.1111/j.1464-410X.2009.08638.x (DOI)
Available from: 2010-04-06 Created: 2010-04-06 Last updated: 2017-12-12Bibliographically approved
Mohlin, C., Säve, S., Nilsson, M. & Persson, K. (2009). Studies of the Extracellular ATP-Adenosine Pathway in Human Urinary Tract Epithelial Cells. Pharmacology, 84(4), 196-202
Open this publication in new window or tab >>Studies of the Extracellular ATP-Adenosine Pathway in Human Urinary Tract Epithelial Cells
2009 (English)In: Pharmacology, ISSN 0031-7012, E-ISSN 1423-0313, Vol. 84, no 4, p. 196-202Article in journal (Refereed) Published
Abstract [en]

Aims: Extracellular ATP may be metabolized to AMP and adenosine by the ectonucleotidases CD39 and CD73 and, in this study, we characterized the pathways for adenosine formation in human urinary tract epithelial cells. Methods: Bladder (RT4) and kidney (A498) epithelial cells were grown in cell culture and the expression of CD39 and CD73 was investigated by reverse transcription-polymerase chain reaction (RT-PCR) and immunohistochemistry. High-performance liquid chromatography was used to determine adenosine formation in cell medium. Results: RT-PCR and immunohistochemistry revealed a high CD73 and a low CD39 expression in human urinary tract epithelial cells, whereas neutrophils had a higher CD39 than CD73 expression. Adenosine was produced when the cells were exposed to 5'-AMP (substrate for CD73), but not when exposed to 5'-ATP (substrate for CD39). A pronounced inhibition of 5'-AMP-induced adenosine formation by the CD73 inhibitor AMP-CP confirmed the involvement of CD73. Adenosine production from 5'-ATP was slightly increased (p < 0.05) when epithelial cells were cocultured with neutrophils. Conclusions: The data demonstrate that adenosine formation from extracellular ATP is negligible in urinary tract epithelial cells due to low CD39 expression in this cell type. However, the epithelial cells express CD73 and are able to convert extracellular AMP to adenosine.

National Category
Medical and Health Sciences
Research subject
Biomedical Sciences, Pharmacology
Identifiers
urn:nbn:se:lnu:diva-2023 (URN)10.1159/000235908 (DOI)
Available from: 2010-04-06 Created: 2010-04-06 Last updated: 2017-12-12Bibliographically approved
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