CXCL5 drives neutrophil recruitment in TH17-mediated GN

Erik M. Disteldorf, Christian F. Krebs, Hans Joachim Paust, Jan Eric Turner, Geraldine Nouailles, André Tittel, Catherine Meyer-Schwesinger, Gesa Stege, Silke Brix, Joachim Velden, Thorsten Wiech, Udo Helmchen, Oliver M. Steinmetz, Anett Peters, Sabrina B. Bennstein, Anna Kaffke, Chrystel Llanto, Sergio A. Lira, Hans Willi Mittrücker, Rolf A.K. StahlChristian Kurts, Stefan H.E. Kaufmann, Ulf Panzer

Research output: Contribution to journalArticlepeer-review

95 Scopus citations


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.

Original languageEnglish
Pages (from-to)55-66
Number of pages12
JournalJournal of the American Society of Nephrology : JASN
Issue number1
StatePublished - 1 Jan 2015


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