Research ExplorerPublicationsCXCL5 drives neutrophil recruitment in TH17-mediated GN

CXCL5 drives neutrophil recruitment in TH17-mediated GN

Standard

CXCL5 drives neutrophil recruitment in TH17-mediated GN. / Disteldorf, Erik M; Krebs, Christian F; Paust, Hans-Joachim; Turner, Jan-Eric; Nouailles, Geraldine; Tittel, André; Meyer-Schwesinger, Catherine; Stege, Gesa; Brix, Silke; Velden, Joachim; Wiech, Thorsten; Helmchen, Udo; Steinmetz, Oliver M; Peters, Anett; Bennstein, Sabrina B; Kaffke, Anna; Llanto, Chrystel; Lira, Sergio A; Mittrücker, Hans-Willi; Stahl, Rolf A K; Kurts, Christian; Kaufmann, Stefan H E; Panzer, Ulf.

In: J AM SOC NEPHROL, Vol. 26, No. 1, 01.01.2015, p. 55-66.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Disteldorf, EM, Krebs, CF, Paust, H-J, Turner, J-E, 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, Mittrücker, H-W, Stahl, RAK, Kurts, C, Kaufmann, SHE & Panzer, U 2015, 'CXCL5 drives neutrophil recruitment in TH17-mediated GN', J AM SOC NEPHROL, vol. 26, no. 1, pp. 55-66. https://doi.org/10.1681/ASN.2013101061

APA

Disteldorf, E. M., Krebs, C. F., Paust, H-J., Turner, J-E., Nouailles, G., Tittel, A., Meyer-Schwesinger, C., Stege, G., Brix, S., Velden, J., Wiech, T., Helmchen, U., Steinmetz, O. M., Peters, A., Bennstein, S. B., Kaffke, A., Llanto, C., Lira, S. A., Mittrücker, H-W., ... Panzer, U. (2015). CXCL5 drives neutrophil recruitment in TH17-mediated GN. J AM SOC NEPHROL, 26(1), 55-66. https://doi.org/10.1681/ASN.2013101061

Vancouver

Disteldorf EM, Krebs CF, Paust H-J, Turner J-E, Nouailles G, Tittel A et al. CXCL5 drives neutrophil recruitment in TH17-mediated GN. J AM SOC NEPHROL. 2015 Jan 1;26(1):55-66. https://doi.org/10.1681/ASN.2013101061

Bibtex

@article{8010092f32754401a69a792428caead1,
title = "CXCL5 drives neutrophil recruitment in TH17-mediated GN",
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.",
keywords = "Animals, Chemokine CXCL1, Chemokine CXCL5, Chemokines, Disease Models, Animal, Epithelial Cells, Female, Glomerulonephritis, Inflammation, Interleukin-17, Kidney, Kidney Tubules, Male, Mice, Mice, Knockout, Mice, Transgenic, Neutrophil Infiltration, Neutrophils, Th17 Cells, Up-Regulation",
author = "Disteldorf, {Erik M} and Krebs, {Christian F} and Hans-Joachim Paust and Jan-Eric Turner and Geraldine Nouailles and Andr{\'e} Tittel and Catherine Meyer-Schwesinger and Gesa Stege and Silke Brix and Joachim Velden and Thorsten Wiech and Udo Helmchen and Steinmetz, {Oliver M} and Anett Peters and Bennstein, {Sabrina B} and Anna Kaffke and Chrystel Llanto and Lira, {Sergio A} and Hans-Willi Mittr{\"u}cker and Stahl, {Rolf A K} and Christian Kurts and Kaufmann, {Stefan H E} and Ulf Panzer",
note = "Copyright {\textcopyright} 2015 by the American Society of Nephrology.",
year = "2015",
month = jan,
day = "1",
doi = "10.1681/ASN.2013101061",
language = "English",
volume = "26",
pages = "55--66",
journal = "J AM SOC NEPHROL",
issn = "1046-6673",
publisher = "American Society of Nephrology",
number = "1",

}

RIS

TY - JOUR

T1 - CXCL5 drives neutrophil recruitment in TH17-mediated GN

AU - Disteldorf, Erik M

AU - Krebs, Christian F

AU - Paust, Hans-Joachim

AU - Turner, Jan-Eric

AU - Nouailles, Geraldine

AU - Tittel, André

AU - Meyer-Schwesinger, Catherine

AU - Stege, Gesa

AU - Brix, Silke

AU - Velden, Joachim

AU - Wiech, Thorsten

AU - Helmchen, Udo

AU - Steinmetz, Oliver M

AU - Peters, Anett

AU - Bennstein, Sabrina B

AU - Kaffke, Anna

AU - Llanto, Chrystel

AU - Lira, Sergio A

AU - Mittrücker, Hans-Willi

AU - Stahl, Rolf A K

AU - Kurts, Christian

AU - Kaufmann, Stefan H E

AU - Panzer, Ulf

N1 - Copyright © 2015 by the American Society of Nephrology.

PY - 2015/1/1

Y1 - 2015/1/1

N2 - 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.

AB - 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.

KW - Animals

KW - Chemokine CXCL1

KW - Chemokine CXCL5

KW - Chemokines

KW - Disease Models, Animal

KW - Epithelial Cells

KW - Female

KW - Glomerulonephritis

KW - Inflammation

KW - Interleukin-17

KW - Kidney

KW - Kidney Tubules

KW - Male

KW - Mice

KW - Mice, Knockout

KW - Mice, Transgenic

KW - Neutrophil Infiltration

KW - Neutrophils

KW - Th17 Cells

KW - Up-Regulation

U2 - 10.1681/ASN.2013101061

DO - 10.1681/ASN.2013101061

M3 - SCORING: Journal article

C2 - 24904089

VL - 26

SP - 55

EP - 66

JO - J AM SOC NEPHROL

JF - J AM SOC NEPHROL

SN - 1046-6673

IS - 1

ER -