Expression of intercellular adhesion molecule‐1 and vascular cell adhesion molecule‐1 in human crescentic glomerulonephritis

Moon, Kyung Chul; Park, So Yeon; Kim, H W; Hong, Hye Kyoung; Lee, H S

doi:10.1046/j.1365-2559.2002.01446.x

Cited by 18 publications

(10 citation statements)

References 26 publications

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“…TNF induces ICAM-1 expression on tubular epithelial cells (42), mesangial cells (43), and glomerular epithelial cells (44). ICAM-1 expression is induced by INF-␥ (45), reactive oxygen species (ROS) (46), and IL-1 (47).…”

Section: Discussionmentioning

confidence: 99%

Intrinsic Renal Cells Are the Major Source of Tumor Necrosis Factor Contributing to Renal Injury in Murine Crescentic Glomerulonephritis

Timoshanko¹,

Sedgwick²,

Holdsworth³

et al. 2003

Journal of the American Society of Nephrology

108

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Abstract. Macrophages are prominent participants in crescentic glomerulonephritis (GN) and have been suggested to be the major source of TNF in this cell-mediated form of glomerular inflammation. Intrinsic renal cells also have the capacity to produce TNF. For dissecting the contribution of local versus bone marrow (BM)-derived TNF in inflammatory renal injury, TNF chimeric mice were created by transplanting normal wildtype (WT) BM into irradiated TNF-deficient recipients (WT3 TNF Ϫ/Ϫ chimeras) and vice versa (TNF Ϫ/Ϫ 3 WT chimeras). A model of crescentic GN induced by an intravenous injection of sheep anti-murine glomerular basement membrane antibody was studied in WT mice, mice with complete TNF deficiency (TNFϪ/Ϫ), and chimeric mice. Crescentic GN was attenuated in TNFϪ/Ϫ mice with fewer crescents (crescents, 13.7 Ϯ 1.7% of glomeruli) and reduced functional indices of renal injury (serum creatinine, 15.2 Ϯ 0.8 mol/L). Similar protection (crescents, 14.3 Ϯ 1.9% of glomeruli; serum creatinine, 18.9 Ϯ 1.1 mol/L) was observed in chimeric mice with intact BM but absent renal-derived TNF (WT3 TNF Ϫ/Ϫ chimeras), suggesting a minor contribution of infiltrating leukocytes to TNF-mediated renal injury. Chimeric mice with TNFdeficient leukocytes but intact intrinsic renal cell-derived TNF (crescents, 20.5 Ϯ 2.0% of glomeruli; serum creatinine, 21.6 Ϯ 1.4 mol/L) developed similar crescentic GN to WT mice (crescents, 22.3 Ϯ 1.4% of glomeruli; serum creatinine, 24.8 Ϯ 1.9 mol/L). Cutaneous delayed-type hypersensitivity after subdermal challenge with the nephritogenic antigen was attenuated in the absence of BM cell-derived TNF but unaffected in WT3 TNF Ϫ/Ϫ chimeric mice. These studies suggest that intrinsic renal cells are the major cellular source of TNF contributing to inflammatory injury in crescentic GN.

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Section: Discussionmentioning

confidence: 99%

Intrinsic Renal Cells Are the Major Source of Tumor Necrosis Factor Contributing to Renal Injury in Murine Crescentic Glomerulonephritis

Timoshanko¹,

Sedgwick²,

Holdsworth³

et al. 2003

Journal of the American Society of Nephrology

108

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“…In addition, activation of neutrophils with ANCA causes a conformational change in ␤ integrins that enhances ligand binding (37). A role for adhesion molecules in the interaction between ANCA-activated neutrophils and vessels also is supported by the immunohistologic evidence for upregulated adhesion molecules in glomerular lesions in renal biopsy specimens from patients with ANCA disease (38).…”

Section: Neutrophil and Monocyte Activation By Anca In Vitromentioning

confidence: 96%

Pathogenesis of Vascular Inflammation by Anti-Neutrophil Cytoplasmic Antibodies

Jennette¹,

Xiao²,

Falk³

2006

Journal of the American Society of Nephrology

185

126

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The reports of a newborn who developed glomerulonephritis and pulmonary hemorrhage after transplacental transfer of anti-neutrophil cytoplasmic antibody (ANCA) IgG with specificity for myeloperoxidase (MPO) is compelling clinical evidence that ANCA are pathogenic. In vitro studies indicate that ANCA activate cytokine-primed neutrophils and monocytes through both direct Fab2 binding and Fc receptor engagement. Neutrophils that have been activated by ANCA release oxygen radicals, lytic enzymes, and inflammatory cytokines and adhere to and kill endothelial cells. A murine model caused by passive administration of mouse anti-mouse MPO IgG provides convincing evidence that ANCA IgG alone in the absence of antigen-specific T cells can cause necrotizing glomerulonephritis and vasculitis. This pathogenic process is enhanced by synergistic inflammatory factors, probably through priming of neutrophils. Immunization of rats with human MPO induces antibodies that cross-react with rat MPO and cause glomerulonephritis and vasculitis. These ANCA act in concert with chemokines to cause adherence of leukocytes to the walls of small vessels with subsequent injury. To date, animal models of disease that is induced by anti-proteinase 3 are less robust. Clinical and experimental data suggest but do not prove that the ANCA autoimmune response is initiated by an immune response to an antisense peptide of the ANCA antigen or its mimic that may be introduced into the body by an infectious pathogen. This antibody response elicits anti-idiotypic antibodies that cross-react with ANCA antigens. The pathogenesis of ANCA disease is multifactorial, with genetic and environmental factors influencing onset of the autoimmune response, the mediation of acute injury, and the induction of the chronic response to injury.

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“…38 -40 Also ICAM-1 was upregulated in MCs by poly(I:C) RNA, a finding of interest because this adhesion molecule is up-regulated and plays a significant role in glomerulonephritis. 41 Furthermore, M-CSF mRNA levels were increased by poly(I:C) RNA exposure of MCs. M-CSF generation by MCs under basal and immune complex-stimulated conditions 42,43 and glomerular CSF expression glomerulonephritis 44 have been reported in and correlate with renal macrophage accumulation as well as glomerular injury and proteinuria.…”

Section: Toll-like Receptor 3 and Glomerulonephritis 381mentioning

confidence: 96%

“…50 M-CSF would sustain and activate the monocytes 46 to macrophages and ICAM-1 favor their glomerular infiltration. 41 The potential role of IL-6 in this hypothetical scenario is less clear but could influence the overall immune response and especially the Th2 response and determine potential chronicity. [55][56][57] Although the effects of poly(I:C) RNA on chemokine and cytokine generation by cytokine-conditioned MCs would fit into the general scheme of glomerular immune injury, how about the anti-proliferative, proapoptotic effects of poly(I:C) RNA observed in our study?…”

Section: Toll-like Receptor 3 and Glomerulonephritis 381mentioning

confidence: 99%