Please use this identifier to cite or link to this item: http://hdl.handle.net/2381/46087
Title: Absence of the Lectin Activation Pathway of Complement Ameliorates Proteinuria-Induced Renal Injury.
Authors: Alghadban, Samy
Kenawy, Hany I.
Dudler, Thomas
Schwaeble, Wilhelm J.
Brunskill, Nigel J.
First Published: 23-Sep-2019
Publisher: Frontiers Media
Citation: Frontiers in Immunology, 2019, 10:2238
Abstract: Proteinuria is an adverse prognostic feature in renal diseases. In proteinuric nephropathies, filtered proteins exert an injurious effect on the renal tubulointerstitium, resulting in inflammation and fibrosis. In the present study, we assessed to what extent complement activation via the lectin pathway may contribute to renal injury in response to proteinuria-related stress in proximal tubular cells. We used the well-established mouse model of protein overload proteinuria (POP) to assess the effect of lectin pathway inhibition on renal injury and fibrotic changes characteristic of proteinuric nephropathy. To this end, we compared experimental outcomes in wild type mice with MASP-2-deficient mice or wild type mice treated with MASP-2 inhibitor to block lectin pathway functional activity. Multiple markers of renal injury were assessed including renal function, proteinuria, macrophage infiltration, and cytokine release profiles. Both MASP-2-deficient and MASP-2 inhibitor-treated wild type mice exhibited renoprotection from proteinuria with significantly less tubulointerstitial injury when compared to isotype control antibody treated mice. This indicates that therapeutic targeting of MASP-2 in proteinuric nephropathies may offer a useful strategy in the clinical management of proteinuria associated pathologies in a variety of different underlying renal diseases.
DOI Link: 10.3389/fimmu.2019.02238
eISSN: 1664-3224
Links: https://www.frontiersin.org/articles/10.3389/fimmu.2019.02238/full
http://hdl.handle.net/2381/46087
Version: Publisher Version
Status: Peer-reviewed
Type: Journal Article
Rights: Copyright © the authors, 2019. This is an open-access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Description: The Supplementary Material for this article can be found online at: https://www.frontiersin.org/articles/10.3389/fimmu.2019.02238/full#supplementary-material
Appears in Collections:Published Articles, Dept. of Infection, Immunity and Inflammation

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