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Updated: Jun 22, 2025
Assessment of Kidney Function in Mouse Models of Glomerular Disease
Published on: June 30, 2018
Expression and significance of Fractalkine/CX3CL1 in MPO-AAV-associated glomerulonephritis rats
Junxue Ma1, Junjie Wang2, Hongli Kang3
1Department of Nephrology, The people's hospital of Baise, Baise, China.
Objective:
To investigate the expression and significance of Fractalkine (CX3CL1, FKN) in serum and renal tissue of myeloperoxidase and anti-neutrophil cytoplasmic antibody associated vasculitis (MPO-AAV) rats.
Methods:
Thirty Wistar-Kyoto (WKY) rats were randomly divided into: Control group, MPO-AAV group (400 µg/kg MPO mixed with Freund's complete adjuvant i.p), MPO-AAV + Anti-FKN group (400 µg/kg MPO mixed with Freund's complete adjuvant i.p), anti-FKN group (1 µg/ rat /day, i.p) after 6 weeks. MPO-AAV associated glomerulonephritis model was established by intraperitoneal injection of MPO + Freund's complete adjuvant with 10 mice in each group. The concentration of MPO-ANCA and FKN in serum was detected by Enzyme-linked immunosorbent assay (ELISA). Hematoxylin-eosin (HE) staining was used to detect pathological changes of kidney tissue. Western blot and immunofluorescence staining were used to detect the expression and localization of FKN protein in kidney tissue. Renal function test indicators: 24-hour urinary protein (UAER), blood urea nitrogen (BUN), serum creatinine (Scr). The expression levels of p65NF-κB and IL-6 was detected by Immunohistochemical assays.
Results:
Compared with the control group, the serum MPO-ANCA antibody expression level in the MPO-AAV group was significantly increased (P < 0.01), and the contents of UAER, BUN and Scr were significantly up-regulated at 24 h (P < 0.01). Compared with the control group, the glomeruli in the MPO-AAV group had different degrees of damage, infiltration of inflammatory cell, and membrane cell hyperplasia and renal tubule edema. Compared with the control group, rats in the MPO-AAV group had significantly higher levels of FKN in serum and renal tissues (P < 0.01), and high expression of p65NF-κB and IL-6 in renal tissues (P < 0.01) (P < 0.05), whereas anti-FKN reversed the expression of the above factors. In MPO-AAV renal tissue, FKN was mainly expressed in the cytoplasm of renal tubular epithelial cells and glomerular podocytes. In addition, the contents of 24 h UAER, BUN and Scr of renal function in MPO-AAV rats were significantly decreased (P < 0.01) and the damage of renal tissue was significantly ameliorated after the administration of antagonistic FKN.
Conclusion:
FKN may play a key role in the pathogenesis of MPO-AAV associated glomerulonephritis.
Insights
Fractalkine (FKN) is elevated in myeloperoxidase and anti-neutrophil cytoplasmic antibody-associated vasculitis (MPO-AAV) and contributes to kidney damage. Blocking FKN reduced inflammation and improved renal function in MPO-AAV rats.
Area of Science:
- Nephrology
- Immunology
- Pathology
Background:
- Myeloperoxidase and anti-neutrophil cytoplasmic antibody-associated vasculitis (MPO-AAV) is a severe autoimmune disease affecting the kidneys.
- The role of Fractalkine (CX3CL1, FKN) in the pathogenesis of MPO-AAV remains unclear.
Purpose of the Study:
- To investigate the expression and significance of Fractalkine (FKN) in serum and renal tissue of MPO-AAV rats.
- To evaluate the therapeutic potential of anti-FKN treatment in MPO-AAV.
Main Methods:
- An MPO-AAV rat model was established using MPO and Freund's complete adjuvant.
- Serum and kidney tissue levels of MPO-ANCA, FKN, p65NF-κB, and IL-6 were measured using ELISA and immunohistochemistry.
- Renal function was assessed by measuring 24-hour urinary protein (UAER), blood urea nitrogen (BUN), and serum creatinine (Scr).
Main Results:
- MPO-AAV rats exhibited significantly increased serum MPO-ANCA, FKN, p65NF-κB, and IL-6 levels compared to controls.
- Renal tissue showed glomerular damage, inflammatory cell infiltration, and tubular edema in MPO-AAV rats.
- Administration of anti-FKN significantly reduced MPO-ANCA, FKN, p65NF-κB, and IL-6 levels, improved renal function markers, and ameliorated kidney damage.
Conclusions:
- Fractalkine (FKN) plays a crucial role in the pathogenesis of MPO-AAV associated glomerulonephritis.
- Targeting FKN with antagonistic antibodies demonstrates therapeutic potential for MPO-AAV.
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