Interleukin 17 receptor A regulates renal inflammation and aggravates fibrosis

Abstract

Event Abstract Back to Event Interleukin 17 receptor A regulates renal inflammation and aggravates fibrosis Shuwang Ge1, Barbara Hertel1, Hermann Haller1 and Sibylle Von Vietinghoff1* 1 Medizinische Hochschule Hannover, Germany Background: The T cell cytokine IL-17 is an important pro-inflammatory mediator. We have previously shown IL-17 receptor expression on monocytes and a role of IL-17 in macrophage accumulation in peritonitis. We here investigated the role of the IL-17 receptor on myeloid cells in chronic renal inflammation and fibrosis. Methods: Renal interstitial fibrosis was induced by unilateral urethral obstruction in mice reconstituted with Il17ra-/- or control bone marrow or a mixture of both. Renal leukocytes were assessed by flow cytometry, and kidney damage was scored by HE and sirius red staining. Results: Il17ra-/- macrophages were significantly less abundant than wt cells in in the control, and much more markedly the obstructed kidney. Obstruction increased CD11c and F4/80 expression. This phenotype was significantly less pronounced in the cells deficient in IL-17 signaling. The proportion of fibrotic tissue area was significantly lower in mice reconstituted with Il17ra-/- bone marrow than mice with wt bone marrow. Conclusion: Lack of IL-17 receptor A on the myeloid cells significantly alters inflammation and diminishes fibrosis in renal obstruction. Keywords: IL-17, Fibrosis, Monocytes, IL-17 receptor, Inflammation Conference: 15th International Congress of Immunology (ICI), Milan, Italy, 22 Aug - 27 Aug, 2013. Presentation Type: Abstract Topic: Innate immunity Citation: Ge S, Hertel B, Haller H and Von Vietinghoff S (2013). Interleukin 17 receptor A regulates renal inflammation and aggravates fibrosis. Front. Immunol. Conference Abstract: 15th International Congress of Immunology (ICI). doi: 10.3389/conf.fimmu.2013.02.00015 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 08 Mar 2013; Published Online: 22 Aug 2013. * Correspondence: Dr. Sibylle Von Vietinghoff, Medizinische Hochschule Hannover, Hannover, Germany, vonvietinghoff.sibylle@mh-hannover.de Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers Shuwang Ge Barbara Hertel Hermann Haller Sibylle Von Vietinghoff Google Shuwang Ge Barbara Hertel Hermann Haller Sibylle Von Vietinghoff Google Scholar Shuwang Ge Barbara Hertel Hermann Haller Sibylle Von Vietinghoff PubMed Shuwang Ge Barbara Hertel Hermann Haller Sibylle Von Vietinghoff Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.