Mononuclear Cell-Infiltrate Inhibition by Blocking Macrophage-Derived Chemokine Results in Attenuation of Developing Crescentic Glomerulonephritis

García, Georgia Earnest; Xia, Ying; Harrison, Jeffrey K.; Wilson, Curtis B.; Johnson, Richard J.; Bacon, Kevin B.; Li, Feng

doi:10.1016/s0002-9440(10)63903-x

Cited by 37 publications

(47 citation statements)

References 53 publications

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“…13,49 Isolated glomeruli from rats were homogenized in phosphate-buffered saline with protease inhibitors. After centrifugation, the supernatants were collected and enriched by immunoprecipitation.…”

Section: Immunoprecipitation and Western Blot Analysismentioning

confidence: 99%

“…In situ hybridization was performed using paraffin-embedded kidney sections as described previously. 11,13 Rat CXCL16 riboprobe was synthesized with incorporation of 35 S-UTP. After autoradiography for 3 days, the slides were dipped in Kodak NTB2 nuclear emulsion (Eastman Kodak, Rochester, NY) diluted 1:1 with water at 42°C.…”

Section: In Situ Hybridizationmentioning

confidence: 99%

“…A rabbit antiserum to rat glomerular basement membrane was prepared as described. 1,13 At day 0, male WKY rats (Harlan, Indianapolis, IN), weighing 200 to 220 g, received one intravenous injection of anti-GBM Ab at a dose of 25 l/100 g of body weight. Four groups of eight rats each were given either 100 l of anti-CXCL16 RS or normal rabbit serum (NRS) intraperitoneally for a period of 7 days, starting from day 1 after administration of anti-GBM Ab.…”

Section: Induction Blocking Experiment and Analysis Of Anti-gbm Gn mentioning

confidence: 99%

“…17 The chemokine MDC/CCL22 is highly expressed throughout anti-GBM GN and attracts macrophages into the glomeruli. 13 The presence of MDC/CCL22 during the progression of anti-GBM GN could support monocyte/ macrophage infiltration and, hence, might explain why neutralization of CXCL16 did not completely block macrophage infiltration into the glomerulus. We recognize that other chemokines (eg, CCL3/MIP-1␣, CCL4/MIP-1␤, CCL5/RANTES, and CX 3 CL1/fractaline) do promote the inflammatory phase of the disease.…”

Section: Cd8mentioning

confidence: 99%

“…11,12 In WistarKyoto (WKY) rats with anti-GBM GN, CCL2/MCP-1, CCL3/MIP-1␣, CCL4/MIP-1␤, CCL5/RANTES, CCL22/ MDC, and CX 3 CL1/fractalkine are expressed. 1,3,13 In mice with accelerated nephrotoxic serum nephritis, CCL5/RANTES and CCL2/MCP-1 increase in relationship to infiltration of T lymphocytes and macrophages. 4 CCL2/ MCP-1 has also been detected in IgA nephropathy, proliferative GN, lupus nephritis, Wegener's granulomatosis, and acute interstitial nephritis.…”

mentioning

confidence: 99%

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Inhibition of CXCL16 Attenuates Inflammatory and Progressive Phases of Anti-Glomerular Basement Membrane Antibody-Associated Glomerulonephritis

García

Truong

et al. 2007

The American Journal of Pathology

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Chemokines recruit and activate leukocytes during inflammation. CXCL16 is a recently discovered chemokine that is expressed as a transmembrane protein that is cleaved to form the active, soluble chemokine. We analyzed the role of CXCL16 in the development of inflammation and in the progression of the anti-glomerular basement membrane (GBM) antibody-induced experimental glomerulonephritis in WistarKyoto rats. CXCL16 was expressed in glomerular endothelial cells and mediated adhesion of macrophages expressing CXCL16 and its cognate receptor, CXCR6. Glomerular infiltrates displayed a strong migratory response to soluble CXCL16. Soluble CXCL16 and its receptor CXCR6 were induced in nephritic glomeruli throughout the disease, and CXCL16 expression correlated with the up-regulation of ADAM10, suggesting that this disintegrin and metalloproteinase mediates the chemokine activity of CXCL16. Blocking CXCL16 in the acute inflammatory phase or progressive phase of established glomerulonephritis significantly attenuated monocyte/macrophage infiltration and glomerular injury; proteinuria also improved. We conclude that CXCL16/CXCR6 plays a critical role in stimulating leukocyte influx, which causes glomerular damage during anti-GBM glomerulonephritis. Blocking CXCL16 actions limits the progression of anti-GBM glomerulonephritis even when the disease is established.

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Section: Immunoprecipitation and Western Blot Analysismentioning

confidence: 99%

Section: In Situ Hybridizationmentioning

confidence: 99%

Section: Induction Blocking Experiment and Analysis Of Anti-gbm Gn mentioning

confidence: 99%

Section: Cd8mentioning

confidence: 99%

mentioning

confidence: 99%

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Inhibition of CXCL16 Attenuates Inflammatory and Progressive Phases of Anti-Glomerular Basement Membrane Antibody-Associated Glomerulonephritis

García

Truong

et al. 2007

The American Journal of Pathology

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Leukocytes in glomerular injury

Holdsworth

Tipping

2007

Semin Immunopathol

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Leukocytes of the innate immune system play a central protective role in immune defense to pathogens but may also mediate injurious inflammatory responses resulting in tissue injury. These leukocytes provide the first rapid cellular defense mechanisms through a limited repertoire of rapid pre-programmed responses, but they are also involved in chronic inflammation and tissue repair. They are directed to sites of pathogen challenge and inflammation by a variety of mechanisms and are activated in response to both exogenous and endogenous stimuli. They do not show the capacity of self-non-self discrimination and memory, which are defining characteristics of the adaptive immune system, although macrophages in particular may show some capacity for differentiation of their effector responses. However, they do play an integral role in adaptive immune responses by their capacity to present antigen, modify T-cell development, and function as effectors of adaptive cell-mediated immunity.

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Anti-macrophage-derived chemokine antibody relieves murine lupus nephritis

Liu

Diao

et al. 2010

Rheumatol Int

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We observed the distribution of monocyte's changes in damage to renal tissue and the expression of macrophage-derived chemokine (MDC) in MRL/lpr mice. The 8-week-old MRL/lpr mice were randomly assigned to receive either MDC antibodies (n = 6) or placebo (n = 6) at a once-every-other-day dose of 300 μl from week 4. We then quantified the differences in 24-h urine protein and serum creatinine concentrations, performed a histological evaluation of renal tissue and assessed the expression of MDC protein and mRNA between the two groups 4 weeks after treatment was initiated. Antibody-treated mice demonstrated significantly lower urine protein and serum creatinine concentrations and had fewer renal lesions compared with control mice. The expression of MDC protein and mRNA in renal tissues was significantly lower in the antibody-treated mice than in control mice, suggesting that the elevated expression of MDC, which led to monocyte infiltration in the kidney, may play an important role in the development of lupus nephritis. Furthermore, the anti-MDC antibodies may act to alleviate the renal lesions of murine lupus nephritis by inhibiting the infiltration of monocytes in the renal tissue of the lupus mice.

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Mononuclear Cell-Infiltrate Inhibition by Blocking Macrophage-Derived Chemokine Results in Attenuation of Developing Crescentic Glomerulonephritis

Cited by 37 publications

References 53 publications

Inhibition of CXCL16 Attenuates Inflammatory and Progressive Phases of Anti-Glomerular Basement Membrane Antibody-Associated Glomerulonephritis

Inhibition of CXCL16 Attenuates Inflammatory and Progressive Phases of Anti-Glomerular Basement Membrane Antibody-Associated Glomerulonephritis

Leukocytes in glomerular injury

Anti-macrophage-derived chemokine antibody relieves murine lupus nephritis

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