Your browser doesn't support javascript.
loading
Blockade of the G-CSF Receptor Is Protective in a Mouse Model of Renal Ischemia-Reperfusion Injury.
McRae, Jennifer L; Vikstrom, Ingela B; Bongoni, Anjan K; Salvaris, Evelyn J; Fisicaro, Nella; Ng, Milica; Alhamdoosh, Monther; Baz Morelli, Adriana; Cowan, Peter J; Pearse, Martin J.
Afiliación
  • McRae JL; Immunology Research Centre, St. Vincent's Hospital Melbourne, Melbourne, Victoria 3065, Australia.
  • Vikstrom IB; CSL Ltd., Melbourne, Victoria 3052, Australia; and.
  • Bongoni AK; Immunology Research Centre, St. Vincent's Hospital Melbourne, Melbourne, Victoria 3065, Australia.
  • Salvaris EJ; Immunology Research Centre, St. Vincent's Hospital Melbourne, Melbourne, Victoria 3065, Australia.
  • Fisicaro N; Immunology Research Centre, St. Vincent's Hospital Melbourne, Melbourne, Victoria 3065, Australia.
  • Ng M; CSL Ltd., Melbourne, Victoria 3052, Australia; and.
  • Alhamdoosh M; CSL Ltd., Melbourne, Victoria 3052, Australia; and.
  • Baz Morelli A; CSL Ltd., Melbourne, Victoria 3052, Australia; and.
  • Cowan PJ; Immunology Research Centre, St. Vincent's Hospital Melbourne, Melbourne, Victoria 3065, Australia; peter.cowan@svha.org.au.
  • Pearse MJ; Department of Medicine, University of Melbourne, Melbourne, Victoria 3052, Australia.
J Immunol ; 205(5): 1433-1440, 2020 09 01.
Article en En | MEDLINE | ID: mdl-32839213
Ischemia-reperfusion injury (IRI) is a complex inflammatory process that detrimentally affects the function of transplanted organs. Neutrophils are important contributors to the pathogenesis of renal IRI. Signaling by G-CSF, a regulator of neutrophil development, trafficking, and function, plays a key role in several neutrophil-associated inflammatory disease models. In this study, we investigated whether targeting neutrophils with a neutralizing mAb to G-CSFR would reduce inflammation and protect against injury in a mouse model of warm renal IRI. Mice were treated with anti-G-CSFR 24 h prior to 22-min unilateral renal ischemia. Renal function and histology, complement activation, and expression of kidney injury markers, and inflammatory mediators were assessed 24 h after reperfusion. Treatment with anti-G-CSFR protected against renal IRI in a dose-dependent manner, significantly reducing serum creatinine and urea, tubular injury, neutrophil and macrophage infiltration, and complement activation (plasma C5a) and deposition (tissue C9). Renal expression of several proinflammatory genes (CXCL1/KC, CXCL2/MIP-2, MCP-1/CCL2, CXCR2, IL-6, ICAM-1, P-selectin, and C5aR) was suppressed by anti-G-CSFR, as was the level of circulating P-selectin and ICAM-1. Neutrophils in anti-G-CSFR-treated mice displayed lower levels of the chemokine receptor CXCR2, consistent with a reduced ability to traffic to inflammatory sites. Furthermore, whole transcriptome analysis using RNA sequencing showed that gene expression changes in IRI kidneys after anti-G-CSFR treatment were indistinguishable from sham-operated kidneys without IRI. Hence, anti-G-CSFR treatment prevented the development of IRI in the kidneys. Our results suggest G-CSFR blockade as a promising therapeutic approach to attenuate renal IRI.
Asunto(s)

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Daño por Reperfusión / Receptores de Factor Estimulante de Colonias de Granulocito / Sustancias Protectoras / Enfermedades Renales Tipo de estudio: Prognostic_studies Límite: Animals Idioma: En Revista: J Immunol Año: 2020 Tipo del documento: Article País de afiliación: Australia Pais de publicación: Estados Unidos

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Daño por Reperfusión / Receptores de Factor Estimulante de Colonias de Granulocito / Sustancias Protectoras / Enfermedades Renales Tipo de estudio: Prognostic_studies Límite: Animals Idioma: En Revista: J Immunol Año: 2020 Tipo del documento: Article País de afiliación: Australia Pais de publicación: Estados Unidos