Sökning: WFRF:(Schanstra Joost P.) >
Blockade of the kal...
Blockade of the kallikrein-kinin system reduces endothelial complement activation in vascular inflammation
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- Lopatko Fagerström, Ingrid (författare)
- Lund University,Lunds universitet,Pediatrisk nefrologi,Forskargrupper vid Lunds universitet,Pediatric Nephrology,Lund University Research Groups,Lund Univ, Sweden
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- Ståhl, Anne lie (författare)
- Lund University,Lunds universitet,Pediatrisk nefrologi,Forskargrupper vid Lunds universitet,Pediatric Nephrology,Lund University Research Groups,Lund Univ, Sweden
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- Mossberg, Maria (författare)
- Lund University,Lunds universitet,Barninfektioner och global barn- och ungdomshälsa,Forskargrupper vid Lunds universitet,Pediatrik infectious diseases and global child health,Lund University Research Groups,Lund Univ, Sweden
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- Tati, Ramesh (författare)
- Lund University,Lunds universitet,Pediatrisk nefrologi,Forskargrupper vid Lunds universitet,Pediatric Nephrology,Lund University Research Groups,Lund Univ, Sweden
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- Kristoffersson, Ann Charlotte (författare)
- Lund University,Lunds universitet,Pediatrisk nefrologi,Forskargrupper vid Lunds universitet,Pediatric Nephrology,Lund University Research Groups,Lund Univ, Sweden
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- Kahn, Robin (författare)
- Lund University,Lunds universitet,Barnreumatologiskt forskningscentrum,Forskargrupper vid Lunds universitet,WCMM- Wallenberg center för molekylär medicinsk forskning,Medicinska fakulteten,Center of Pediatric Rheumatology,Lund University Research Groups,WCMM-Wallenberg Centre for Molecular Medicine,Faculty of Medicine,Lund Univ, Sweden
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- Bascands, Jean Loup (författare)
- University of Reunion Island,Univ La Reunion, France
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- Klein, Julie (författare)
- Institute of Cardiovascular and Metabolic Diseases (I2MC),Université Paul Sabatier,INSERM, France; Univ Toulouse III Paul Sabatier, France
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- Schanstra, Joost P. (författare)
- Université Paul Sabatier,Institute of Cardiovascular and Metabolic Diseases (I2MC),INSERM, France; Univ Toulouse III Paul Sabatier, France
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- Segelmark, Mårten (författare)
- Linköpings universitet,Linköping University,Lund University,Lunds universitet,Njurmedicin,Sektion II,Institutionen för kliniska vetenskaper, Lund,Medicinska fakulteten,Nephrology,Section II,Department of Clinical Sciences, Lund,Faculty of Medicine,Avdelningen för läkemedelsforskning,Region Östergötland, Njurmedicinska kliniken US,Lund Univ, Sweden
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- Karpman, Diana (författare)
- Lund University,Lunds universitet,Pediatrisk nefrologi,Forskargrupper vid Lunds universitet,Pediatric Nephrology,Lund University Research Groups,Lund Univ, Sweden
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(creator_code:org_t)
- Elsevier BV, 2019
- 2019
- Engelska.
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Ingår i: EBioMedicine. - : Elsevier BV. - 2352-3964. ; 47, s. 319-328
- Relaterad länk:
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http://dx.doi.org/10... (free)
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http://www.thelancet...
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https://liu.diva-por... (primary) (Raw object)
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https://lup.lub.lu.s...
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https://doi.org/10.1...
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https://urn.kb.se/re...
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Abstract
Ämnesord
Stäng
- Background: The complement and kallikrein-kinin systems (KKS) are activated during vascular inflammation. The aim of this study was to investigate if blockade of the KKS can affect complement activation on the endothelium during inflammation. Methods: Complement deposition on endothelial microvesicles was assayed in vasculitis patient plasma samples and controls. Plasma was perfused over glomerular endothelial cells and complement deposition assayed by flow cytometry. The effect of the kinin system was assessed using kinin receptor antagonists and C1-inhibitor. The in vivo effect was assessed in kidney sections from mice with nephrotoxic serum-induced glomerulonephritis treated with a kinin receptor antagonist. Findings: Vasculitis patient plasma had significantly more C3- and C9-positive endothelial microvesicles than controls. Perfusion of patient acute-phase plasma samples over glomerular endothelial cells induced the release of significantly more complement-positive microvesicles, in comparison to remission or control plasma. Complement activation on endothelial microvesicles was reduced by kinin B1- and B2-receptor antagonists or by C1-inhibitor (the main inhibitor of the classical pathway and the KKS). Likewise, perfusion of glomerular endothelial cells with C1-inhibitor-depleted plasma induced the release of complement-positive microvesicles, which was significantly reduced by kinin-receptor antagonists or C1-inhibitor. Mice with nephrotoxic serum-induced glomerulonephritis exhibited significantly reduced glomerular C3 deposition when treated with a B1-receptor antagonist. Interpretation: Excessive complement deposition on the endothelium will promote endothelial injury and the release of endothelial microvesicles. This study demonstrates that blockade of the KKS can reduce complement activation and thereby the inflammatory response on the endothelium. Funding: Full details are provided in the Acknowledgements/Funding section.
Ämnesord
- MEDICIN OCH HÄLSOVETENSKAP -- Klinisk medicin -- Urologi och njurmedicin (hsv//swe)
- MEDICAL AND HEALTH SCIENCES -- Clinical Medicine -- Urology and Nephrology (hsv//eng)
- MEDICIN OCH HÄLSOVETENSKAP -- Klinisk medicin -- Radiologi och bildbehandling (hsv//swe)
- MEDICAL AND HEALTH SCIENCES -- Clinical Medicine -- Radiology, Nuclear Medicine and Medical Imaging (hsv//eng)
Nyckelord
- Complement
- Endothelial microvesicles
- Kidney
- Kinin
- Mouse
- Vasculitis
- Vasculitis; Endothelial microvesicles; Complement; Kinin; Kidney; Mouse
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Lopatko Fagerstr ...
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Ståhl, Anne lie
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Mossberg, Maria
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Tati, Ramesh
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Kristoffersson, ...
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Kahn, Robin
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Bascands, Jean L ...
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Klein, Julie
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Schanstra, Joost ...
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Segelmark, Mårte ...
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Karpman, Diana
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