CXCL5 drives neutrophil recruitment in TH17-mediated GN
Disteldorf EM, Krebs CF, Paust HJ, Turner JE, Nouailles G, Tittel A, Meyer-Schwesinger C, Stege G, Brix S, Velden J, Wiech T, Helmchen U, Steinmetz OM, Peters A, Bennstein SB, Kaffke A, Llanto C, Lira SA, Mittruecker HW, Stahl RAK, Kurts C, Kaufmann SHE, Panzer U (2015)
Publication Type: Journal article
Publication year: 2015
Journal
Book Volume: 26
Pages Range: 55-66
Journal Issue: 1
Abstract
Neutrophil trafficking to sites of inflammation is essential for the defense against bacterial and fungal infections, but also contributes to tissue damage in TH17-mediated autoimmunity. This process is regulated by chemokines, which often show an overlapping expression pattern and function in pathogen- and autoimmune-induced inflammatory reactions. Using a murine model of crescentic GN, we show that the pathogenic TH17/IL-17 immune response induces chemokine (C-X-C motif) ligand 5 (CXCL5) expression in kidney tubular cells, which recruits destructive neutrophils that contribute to renal tissue injury. By contrast, CXCL5 was dispensable for neutrophil recruitment and effective bacterial clearance in a murine model of acute bacterial pyelonephritis. In line with these findings, CXCL5 expression was highly upregulated in the kidneys of patients with ANCA-associated crescentic GN as opposed to patients with acute bacterial pyelonephritis. Our data therefore identify CXCL5 as a potential therapeutic target for the restriction of pathogenic neutrophil infiltration in TH17-mediated autoimmune diseases while leaving intact the neutrophil function in protective immunity against invading pathogens.
Involved external institutions
Universitätsklinikum Hamburg-Eppendorf (UKE)
Germany (DE)
Max-Planck-Institut für Infektionsbiologie / Max Planck Institute for Infection Biology
Germany (DE)
Universitätsklinikum Bonn
Germany (DE)
Icahn School of Medicine at Mount Sinai
United States (USA) (US)
Germany (DE)
Max-Planck-Institut für Infektionsbiologie / Max Planck Institute for Infection Biology
Germany (DE)
Universitätsklinikum Bonn
Germany (DE)
Icahn School of Medicine at Mount Sinai
United States (USA) (US)
How to cite
APA:
Disteldorf, E.M., Krebs, C.F., Paust, H.-J., Turner, J.-E., Nouailles, G., Tittel, A.,... Panzer, U. (2015). CXCL5 drives neutrophil recruitment in TH17-mediated GN. Journal of the American Society of Nephrology, 26(1), 55-66. https://dx.doi.org/10.1681/ASN.2013101061
MLA:
Disteldorf, Erik M., et al. "CXCL5 drives neutrophil recruitment in TH17-mediated GN." Journal of the American Society of Nephrology 26.1 (2015): 55-66.
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