Effect of granulocyte colony–stimulating factor administration on renal regeneration after experimentally induced acute kidney injury in dogs

2016 ◽  
Vol 77 (2) ◽  
pp. 199-207
Author(s):  
Chae-Young Lim ◽  
Jae-Ik Han ◽  
Seung-Gon Kim ◽  
Chang-Min Lee ◽  
Hee-Myung Park
Keyword(s):  
Acute Kidney Injury ◽  
Kidney Injury ◽  
Granulocyte Colony Stimulating Factor ◽  
Colony Stimulating Factor ◽  
Renal Regeneration ◽  
Stimulating Factor ◽  
Experimentally Induced

scholarly journals Interleukin-18 binding protein transgenic mice are protected against ischemic acute kidney injury

2008 ◽  
Vol 295 (5) ◽  
pp. F1414-F1421 ◽  
Author(s):  
Zhibin He ◽  
Lawrence Lu ◽  
Christopher Altmann ◽  
Thomas S. Hoke ◽  
Danica Ljubanovic ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Binding Protein ◽  
Kidney Injury ◽  
Macrophage Infiltration ◽  
Colony Stimulating Factor ◽  
Wild Type ◽  
Macrophage Colony Stimulating Factor ◽  
Ischemic Acute Kidney Injury ◽  
Macrophage Colony ◽  
Stimulating Factor

IL-18 function is neutralized in IL-18 binding protein transgenic (IL-18BP Tg) mice. First, we determined whether IL-18BP Tg mice are protected against ischemic acute kidney injury (AKI). Ischemic AKI was induced by bilateral renal pedicle clamping. IL-18BP Tg mice were functionally and histologically protected against ischemic AKI as determined by blood urea nitrogen, serum creatinine, and acute tubular necrosis score. We have demonstrated that the injurious effect of IL-18 in the kidney is independent of neutrophils and lymphocytes. Thus the effect of IL-18 inhibition on renal macrophage infiltration was determined. The number of macrophages was significantly reduced in IL-18BP Tg compared with wild-type kidneys. To determine the cytokines and chemokines that are dependent on IL-18, we performed flow cytometry based assays. Multiple chemokines/cytokines, IL-3, IL-6, IL-15, IL-18, leukemia inhibitory factor, macrophage colony-stimulating factor, macrophage inflammatory protein-2, granulocyte-macrophage colony-stimulating factor, and monocyte chemotactic protein-1 were significantly increased in AKI vs. sham kidneys. Only CXCL1 (also known as KC or IL-8) was significantly increased in AKI vs. sham kidneys and significantly reduced in IL-18BP Tg AKI vs. wild-type AKI kidneys. To determine whether macrophages are the source of CXCL1 in the kidney, we depleted macrophages with liposomal encapsulated clodronate. CXCL1 was significantly decreased in macrophage-depleted vs. control AKI mice. In summary, in ischemic AKI in mice, 1) IL-18BP Tg mice are functionally and histologically protected, 2) macrophage infiltration in the kidney and CXCL1 are significantly reduced in IL-18BP Tg mice, and 3) macrophage depletion significantly reduces CXCL1 in the kidney. In conclusion, protection against ischemic AKI in IL-18BP Tg mice is associated with less macrophage infiltration and less production of CXCL1 in the kidney.

Granulocyte-colony stimulating factor for the treatment of neurodegenerative diseases

2008 ◽  
Vol 35 (S 01) ◽  
Author(s):  
T Frank ◽  
K Meuer ◽  
C Pitzer ◽  
J Schulz ◽  
M Bähr ◽  
...  
Keyword(s):  
Neurodegenerative Diseases ◽  
Granulocyte Colony Stimulating Factor ◽  
Colony Stimulating Factor ◽  
Stimulating Factor
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