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  1. Article ; Online: Calcineurin inhibitor Tacrolimus impairs host immune response against urinary tract infection.

    Emal, Diba / Rampanelli, Elena / Claessen, Nike / Bemelman, Frederike J / Leemans, Jaklien C / Florquin, Sandrine / Dessing, Mark C

    Scientific reports

    2019  Volume 9, Issue 1, Page(s) 106

    Abstract: Calcineurin inhibitor Tacrolimus, is a potent immunosuppressive drug widely used in order to prevent acute graft rejection. Urinary tract infection (UTI) is the most frequent infectious complication in renal transplant patients and long-term use of ... ...

    Abstract Calcineurin inhibitor Tacrolimus, is a potent immunosuppressive drug widely used in order to prevent acute graft rejection. Urinary tract infection (UTI) is the most frequent infectious complication in renal transplant patients and long-term use of Tacrolimus might be involved in higher susceptibility to bacterial infections. It remains largely unknown how Tacrolimus affects the host innate immune response against lower and upper UTI. To address this issue, we used experimental UTI model by intravesical inoculation of uropathogenic E.coli in female wild-type mice pre-treated with Tacrolimus or solvent (CTR). We found that Tacrolimus pre-treated mice displayed higher bacterial loads (cystitis, pyelonephritis and bacteremia) than CTR mice. Granulocytes from Tacrolimus pre-treated mice phagocytized less E. coli, released less MPO and expressed decreased levels of CXCR2 receptor upon infection. Moreover, Tacrolimus reduced TLR5 expression in bladder macrophages during UTI. This immunosuppressive state can be explained by the upregulation of TLR-signaling negative regulators (A20, ATF3, IRAK-M and SOCS1) and parallel downregulation of TLR5 as observed in Tacrolimus treated granulocytes and macrophages. We conclude that Tacrolimus impairs host innate immune responses against UTI.
    MeSH term(s) Animals ; Bacterial Load ; Calcineurin Inhibitors/administration & dosage ; Calcineurin Inhibitors/adverse effects ; Disease Models, Animal ; Escherichia coli Infections/immunology ; Escherichia coli Infections/pathology ; Female ; Granulocytes/drug effects ; Granulocytes/immunology ; Immunologic Factors/metabolism ; Immunosuppressive Agents/administration & dosage ; Immunosuppressive Agents/adverse effects ; Mice ; Peroxidase/metabolism ; Phagocytosis/drug effects ; Tacrolimus/administration & dosage ; Tacrolimus/adverse effects ; Urinary Tract Infections/immunology ; Urinary Tract Infections/pathology ; Uropathogenic Escherichia coli/growth & development ; Uropathogenic Escherichia coli/immunology
    Chemical Substances Calcineurin Inhibitors ; Immunologic Factors ; Immunosuppressive Agents ; Peroxidase (EC 1.11.1.7) ; Tacrolimus (WM0HAQ4WNM)
    Language English
    Publishing date 2019-01-14
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2615211-3
    ISSN 2045-2322 ; 2045-2322
    ISSN (online) 2045-2322
    ISSN 2045-2322
    DOI 10.1038/s41598-018-37482-x
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Release of extracellular DNA influences renal ischemia reperfusion injury by platelet activation and formation of neutrophil extracellular traps.

    Jansen, Marcel P B / Emal, Diba / Teske, Gwendoline J D / Dessing, Mark C / Florquin, Sandrine / Roelofs, Joris J T H

    Kidney international

    2017  Volume 91, Issue 2, Page(s) 352–364

    Abstract: Acute kidney injury is often the result of ischemia reperfusion injury, which leads to activation of coagulation and inflammation, resulting in necrosis of renal tubular epithelial cells. Platelets play a central role in coagulation and inflammatory ... ...

    Abstract Acute kidney injury is often the result of ischemia reperfusion injury, which leads to activation of coagulation and inflammation, resulting in necrosis of renal tubular epithelial cells. Platelets play a central role in coagulation and inflammatory processes, and it has been shown that platelet activation exacerbates acute kidney injury. However, the mechanism of platelet activation during ischemia reperfusion injury and how platelet activation leads to tissue injury are largely unknown. Here we found that renal ischemia reperfusion injury in mice leads to increased platelet activation in immediate proximity of necrotic cell casts. Furthermore, platelet inhibition by clopidogrel decreased cell necrosis and inflammation, indicating a link between platelet activation and renal tissue damage. Necrotic tubular epithelial cells were found to release extracellular DNA, which, in turn, activated platelets, leading to platelet-granulocyte interaction and formation of neutrophil extracellular traps ex vivo. Renal ischemia reperfusion injury resulted in increased DNA-platelet and DNA-platelet-granulocyte colocalization in tissue and elevated levels of circulating extracellular DNA and platelet factor 4 in mice. After renal ischemia reperfusion injury, neutrophil extracellular traps were formed within renal tissue, which decreased when mice were treated with the platelet inhibitor clopidogrel. Thus, during renal ischemia reperfusion injury, necrotic cell-derived DNA leads to platelet activation, platelet-granulocyte interaction, and subsequent neutrophil extracellular trap formation, leading to renal inflammation and further increase in tissue injury.
    MeSH term(s) Animals ; Blood Platelets/drug effects ; Blood Platelets/metabolism ; Cell Line ; DNA/genetics ; DNA/metabolism ; Disease Models, Animal ; Epithelial Cells/drug effects ; Epithelial Cells/metabolism ; Epithelial Cells/pathology ; Extracellular Traps/metabolism ; Humans ; Kidney Tubular Necrosis, Acute/genetics ; Kidney Tubular Necrosis, Acute/metabolism ; Kidney Tubular Necrosis, Acute/pathology ; Kidney Tubular Necrosis, Acute/prevention & control ; Kidney Tubules/drug effects ; Kidney Tubules/metabolism ; Kidney Tubules/pathology ; Male ; Mice, Inbred C57BL ; Nephritis/genetics ; Nephritis/metabolism ; Nephritis/pathology ; Platelet Activation/drug effects ; Platelet Aggregation Inhibitors/pharmacology ; Platelet Factor 4/metabolism ; Reperfusion Injury/genetics ; Reperfusion Injury/metabolism ; Reperfusion Injury/pathology ; Reperfusion Injury/prevention & control ; Signal Transduction ; Ticlopidine/analogs & derivatives ; Ticlopidine/pharmacology ; Time Factors
    Chemical Substances Platelet Aggregation Inhibitors ; Platelet Factor 4 (37270-94-3) ; DNA (9007-49-2) ; clopidogrel (A74586SNO7) ; Ticlopidine (OM90ZUW7M1)
    Language English
    Publishing date 2017-02
    Publishing country United States
    Document type Journal Article
    ZDB-ID 120573-0
    ISSN 1523-1755 ; 0085-2538
    ISSN (online) 1523-1755
    ISSN 0085-2538
    DOI 10.1016/j.kint.2016.08.006
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 797: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

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  3. Article ; Online: Corrigendum: Effect of TREM-1 blockade and single nucleotide variants in experimental renal injury and kidney transplantation.

    Tammaro, Alessandra / Kers, Jesper / Emal, Diba / Stroo, Ingrid / Teske, Gwendoline J D / Butter, Loes M / Claessen, Nike / Damman, Jeffrey / Derive, Marc / Navis, Gerjan J / Florquin, Sandrine / Leemans, Jaklien C / Dessing, Mark C

    Scientific reports

    2017  Volume 7, Page(s) 44163

    Language English
    Publishing date 2017-03-15
    Publishing country England
    Document type Journal Article ; Published Erratum
    ZDB-ID 2615211-3
    ISSN 2045-2322 ; 2045-2322
    ISSN (online) 2045-2322
    ISSN 2045-2322
    DOI 10.1038/srep44163
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Monophosphoryl lipid A-induced pro-inflammatory cytokine expression does not require CD14 in primary human dendritic cells.

    Kolanowski, Sonja T H M / Lissenberg-Thunnissen, Suzanne N / Emal, Diba / van Ham, S Marieke / Ten Brinke, Anja

    Inflammation research : official journal of the European Histamine Research Society ... [et al.

    2016  Volume 65, Issue 6, Page(s) 449–458

    Abstract: Objective: To elucidate if TLR4-mediated MyD88 and TRIF signalling by the clinically applicable Lipopolysaccharide (LPS)-derivative monophosphoryl lipid A (MPLA) in primary human dendritic cells requires LPS cofactors LPS-binding protein (LBP) and CD14.! ...

    Abstract Objective: To elucidate if TLR4-mediated MyD88 and TRIF signalling by the clinically applicable Lipopolysaccharide (LPS)-derivative monophosphoryl lipid A (MPLA) in primary human dendritic cells requires LPS cofactors LPS-binding protein (LBP) and CD14.
    Methods: Cytokine production by monocyte-derived DCs stimulated with MPLA or LPS was determined using ELISA. To investigate involvement of CD14 for action of LPS or MPLA, CD14 was inhibited using blocking antibodies or down-modulated using specific siRNA. To assess involvement of LBP monocyte-derived DCs were stimulated in serum-free culture medium in absence or presence of purified LBP.
    Results: LBP and CD14 are not required for and do not enhance the capacity of MPLA to induce MyD88- and TRIF-dependent pro-inflammatory IL-6 and TNF-α. Interestingly, although CD14 is required for TRIF-dependent downstream events in mice, we show that in human CD14 is redundant for MPLA-induced TRIF-dependent chemokine production.
    Conclusions: These findings provide novel insight in the modes of action of MPLA in human and show that, compared to LPS, MyD88 and TRIF signalling in dendritic cells by MPLA is not mediated nor amplified by TLR4 cofactors. This gives insight why MPLA induces immune activation without provoking toxicity in human and clarifies why MPLA can be used as activating compound for clinically applicable immuno-activatory cellular products grown in serum-free regimens.
    MeSH term(s) Acute-Phase Proteins/metabolism ; Adaptor Proteins, Vesicular Transport/metabolism ; Carrier Proteins/metabolism ; Cells, Cultured ; Cytokines/metabolism ; Dendritic Cells/drug effects ; Dendritic Cells/metabolism ; Down-Regulation ; Humans ; Lipid A/analogs & derivatives ; Lipid A/pharmacology ; Lipopolysaccharide Receptors/genetics ; Lipopolysaccharide Receptors/metabolism ; Lipopolysaccharides/pharmacology ; Membrane Glycoproteins/metabolism ; Myeloid Differentiation Factor 88/metabolism ; RNA, Small Interfering/genetics ; Signal Transduction/drug effects
    Chemical Substances Acute-Phase Proteins ; Adaptor Proteins, Vesicular Transport ; Carrier Proteins ; Cytokines ; Lipid A ; Lipopolysaccharide Receptors ; Lipopolysaccharides ; MYD88 protein, human ; Membrane Glycoproteins ; Myeloid Differentiation Factor 88 ; RNA, Small Interfering ; TICAM1 protein, human ; lipopolysaccharide-binding protein ; monophosphoryl lipid A (MWC0ET1L2P)
    Language English
    Publishing date 2016-06
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 1221794-3
    ISSN 1420-908X ; 1023-3830
    ISSN (online) 1420-908X
    ISSN 1023-3830
    DOI 10.1007/s00011-016-0927-0
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 675: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

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  5. Article ; Online: No difference in renal injury and fibrosis between wild-type and NOD1/NOD2 double knockout mice with chronic kidney disease induced by ureteral obstruction.

    Stroo, Ingrid / Emal, Diba / Butter, Loes M / Teske, Gwen J / Claessen, Nike / Dessing, Mark C / Girardin, Stephen E / Florquin, Sandrine / Leemans, Jaklien C

    BMC nephrology

    2018  Volume 19, Issue 1, Page(s) 78

    Abstract: Background: Chronic kidney disease (CKD) is characterized by sustained tissue damage and ongoing tubulo-interstitial inflammation and fibrosis. Pattern recognition receptors (PRRs) including Toll-like receptors (TLRs) and NOD-like receptors (NLRs) can ... ...

    Abstract Background: Chronic kidney disease (CKD) is characterized by sustained tissue damage and ongoing tubulo-interstitial inflammation and fibrosis. Pattern recognition receptors (PRRs) including Toll-like receptors (TLRs) and NOD-like receptors (NLRs) can sense endogenous ligands released upon tissue damage, leading to sterile inflammation and eventually irreversible kidney disease. It is known that NOD1 and NOD2 contribute to the pathogenesis of various inflammatory diseases, including acute kidney injury. However their role in chronic kidney disease is largely unknown. The aim of this study was therefore to investigate the contribution of NOD1 and NOD2 in renal interstitial fibrosis and obstructive nephropathy.
    Methods: To do so, we performed unilateral ureteral obstruction (UUO) in wild type (WT) and NOD1/NOD2 double deficient (DKO) mice and analysed renal damage, fibrosis and inflammation. Data were analysed using the non-parametric Mann-Whitney U-test.
    Results: Minor changes in inflammatory response were observed in NOD1/2 DKO mice, while no effects were observed on renal injury and the development of fibrosis.
    Conclusion: No difference in renal injury and fibrosis between WT and NOD1/NOD2 DKO mice following obstructive nephropathy induced by ureteral obstruction.
    MeSH term(s) Acute Kidney Injury/etiology ; Acute Kidney Injury/genetics ; Acute Kidney Injury/metabolism ; Animals ; Female ; Fibrosis/etiology ; Fibrosis/genetics ; Fibrosis/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Inbred NOD ; Mice, Knockout ; Nod1 Signaling Adaptor Protein/deficiency ; Nod1 Signaling Adaptor Protein/genetics ; Nod2 Signaling Adaptor Protein/deficiency ; Nod2 Signaling Adaptor Protein/genetics ; Renal Insufficiency, Chronic/complications ; Renal Insufficiency, Chronic/genetics ; Renal Insufficiency, Chronic/metabolism ; Ureteral Obstruction/complications ; Ureteral Obstruction/genetics ; Ureteral Obstruction/metabolism
    Chemical Substances Card15 protein, mouse ; Card4 protein, mouse ; Nod1 Signaling Adaptor Protein ; Nod2 Signaling Adaptor Protein
    Language English
    Publishing date 2018-04-02
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2041348-8
    ISSN 1471-2369 ; 1471-2369
    ISSN (online) 1471-2369
    ISSN 1471-2369
    DOI 10.1186/s12882-018-0867-8
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Depletion of Gut Microbiota Protects against Renal Ischemia-Reperfusion Injury.

    Emal, Diba / Rampanelli, Elena / Stroo, Ingrid / Butter, Loes M / Teske, Gwendoline J / Claessen, Nike / Stokman, Geurt / Florquin, Sandrine / Leemans, Jaklien C / Dessing, Mark C

    Journal of the American Society of Nephrology : JASN

    2017  Volume 28, Issue 5, Page(s) 1450–1461

    Abstract: An accumulating body of evidence shows that gut microbiota fulfill an important role in health and disease by modulating local and systemic immunity. The importance of the microbiome in the development of kidney disease, however, is largely unknown. To ... ...

    Abstract An accumulating body of evidence shows that gut microbiota fulfill an important role in health and disease by modulating local and systemic immunity. The importance of the microbiome in the development of kidney disease, however, is largely unknown. To study this concept, we depleted gut microbiota with broad-spectrum antibiotics and performed renal ischemia-reperfusion (I/R) injury in mice. Depletion of the microbiota significantly attenuated renal damage, dysfunction, and remote organ injury and maintained tubular integrity after renal I/R injury. Gut flora-depleted mice expressed lower levels of F4/80 and chemokine receptors CX3CR1 and CCR2 in the F4/80
    MeSH term(s) Animals ; Anti-Bacterial Agents/pharmacology ; Anti-Bacterial Agents/therapeutic use ; CX3C Chemokine Receptor 1 ; Epidermal Growth Factor/physiology ; Gastrointestinal Microbiome/drug effects ; Kidney/blood supply ; Macrophages/physiology ; Male ; Mice ; Mice, Inbred C57BL ; Receptors, Chemokine/physiology ; Reperfusion Injury/microbiology ; Reperfusion Injury/prevention & control
    Chemical Substances Anti-Bacterial Agents ; CX3C Chemokine Receptor 1 ; Cx3cr1 protein, mouse ; Emr4 protein, mouse ; Receptors, Chemokine ; Epidermal Growth Factor (62229-50-9)
    Language English
    Publishing date 2017-05
    Publishing country United States
    Document type Comparative Study ; Journal Article
    ZDB-ID 1085942-1
    ISSN 1533-3450 ; 1046-6673
    ISSN (online) 1533-3450
    ISSN 1046-6673
    DOI 10.1681/ASN.2016030255
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 3344: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

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  7. Article ; Online: Effect of TREM-1 blockade and single nucleotide variants in experimental renal injury and kidney transplantation.

    Tammaro, Alessandra / Kers, Jesper / Emal, Diba / Stroo, Ingrid / Teske, Gwendoline J D / Butter, Loes M / Claessen, Nike / Damman, Jeffrey / Derive, Marc / Navis, Gerjan J / Florquin, Sandrine / Leemans, Jaklien C / Dessing, Mark C

    Scientific reports

    2016  Volume 6, Page(s) 38275

    Abstract: Renal ischemia reperfusion (IR)-injury induces activation of innate immune response which sustains renal injury and contributes to the development of delayed graft function (DGF). Triggering receptor expressed on myeloid cells-1 (TREM-1) is a pro- ... ...

    Abstract Renal ischemia reperfusion (IR)-injury induces activation of innate immune response which sustains renal injury and contributes to the development of delayed graft function (DGF). Triggering receptor expressed on myeloid cells-1 (TREM-1) is a pro-inflammatory evolutionary conserved pattern recognition receptor expressed on a variety of innate immune cells. TREM-1 expression increases following acute and chronic renal injury. However, the function of TREM-1 in renal IR is still unclear. Here, we investigated expression and function of TREM-1 in a murine model of renal IR using different TREM-1 inhibitors: LP17, LR12 and TREM-1 fusion protein. In a human study, we analyzed the association of non-synonymous single nucleotide variants in the TREM1 gene in a cohort comprising 1263 matching donors and recipients with post-transplant outcomes, including DGF. Our findings demonstrated that, following murine IR, renal TREM-1 expression increased due to the influx of Trem1 mRNA expressing cells detected by in situ hybridization. However, TREM-1 interventions by means of LP17, LR12 and TREM-1 fusion protein did not ameliorate IR-induced injury. In the human renal transplant cohort, donor and recipient TREM1 gene variant p.Thr25Ser was not associated with DGF, nor with biopsy-proven rejection or death-censored graft failure. We conclude that TREM-1 does not play a major role during experimental renal IR and after kidney transplantation.
    MeSH term(s) Animals ; Delayed Graft Function/genetics ; Delayed Graft Function/pathology ; Gene Expression Regulation/drug effects ; Humans ; Inflammation/drug therapy ; Inflammation/genetics ; Inflammation/pathology ; Kidney/drug effects ; Kidney/injuries ; Kidney/metabolism ; Kidney/pathology ; Kidney Transplantation/adverse effects ; Lauric Acids/administration & dosage ; Mice ; Polymorphism, Single Nucleotide/genetics ; Recombinant Fusion Proteins/administration & dosage ; Recombinant Fusion Proteins/genetics ; Reperfusion Injury/drug therapy ; Reperfusion Injury/genetics ; Reperfusion Injury/pathology ; Rhodamines/administration & dosage ; Triggering Receptor Expressed on Myeloid Cells-1/antagonists & inhibitors ; Triggering Receptor Expressed on Myeloid Cells-1/genetics
    Chemical Substances Lauric Acids ; Recombinant Fusion Proteins ; Rhodamines ; Triggering Receptor Expressed on Myeloid Cells-1 ; nangibotide (59HD7BLX9H)
    Language English
    Publishing date 2016-12-08
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2615211-3
    ISSN 2045-2322 ; 2045-2322
    ISSN (online) 2045-2322
    ISSN 2045-2322
    DOI 10.1038/srep38275
    Database MEDical Literature Analysis and Retrieval System OnLINE

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