Naive Monocytes Can Trigger Transendothelial Migration of Peripheral Blood Cells Through the Induction of Endothelial Tumour Necrosis Factor‐α

Eißner, Günther; Lindner, Heidrun; Konur, Abdo; Kreutz, Marina; Andreesen, Reinhard; Holler, Ernst

doi:10.1046/j.1365-3083.2000.00677.x

Cited by 6 publications

(6 citation statements)

References 38 publications

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“…In this regard, TNF-a is produced by a broad range of tissues and cells, including immune cells and intrinsic renal cells, such as mesangial cells, 6,17 glomerular 7,8 and tubular epithelial cells, [9][10][11] and endothelial cells. 12,13 As cisplatin nephrotoxicity is associated with the influx of bone marrow-derived inflammatory cells into the kidney, 2,3,9,14 these infiltrating leukocytes could be the source of intrarenal and circulating TNF-a. On the other hand, we have shown that cisplatin stimulates renal epithelial cells to produce TNF-a in vitro 9,14 raising the possibility that renal parenchymal cells are the major source of TNF-a in cisplatin nephrotoxicity.…”

Section: Discussionmentioning

confidence: 99%

“…Several cell types within the kidney are capable of producing TNF-a, 6,7,12,13 including proximal tubule cells. 10,11 We have shown that cisplatin increases TNF-a production by proximal tubule cells in vitro.…”

Section: Discussionmentioning

confidence: 99%

“…TNF-a is produced by a broad range of tissues and cells, including immune cells and intrinsic renal cells, such as mesangial cells, 6 glomerular 7,8 and tubular epithelial cells, [9][10][11] and endothelial cells. 12,13 The extent to which infiltrating immune cells and intrinsic renal cells produce TNF-a and mediate nephrotoxicity in response to cisplatin is not known. Therefore, the purpose of the present study was to determine the relative contribution of TNF-a produced by renal parenchymal cells vs leukocytes in mediating cisplatininduced renal injury in vivo.…”

mentioning

confidence: 99%

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Cisplatin-induced nephrotoxicity is mediated by tumor necrosis factor-α produced by renal parenchymal cells

Zhang

Ramesh

Norbury

et al. 2007

Kidney International

259

188

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Cisplatin is a chemotherapeutic agent that induces tumor necrosis factor-alpha (TNF-alpha) production in many cell types with unfortunate renal toxicity. We sought to determine the contributions of renal parenchymal cells and bone marrow-derived immune cells to the pathogenesis of cisplatin-induced renal injury in vivo. To do this we created chimeric mice in which the bone marrow was ablated and replaced with donor bone marrow cells from wild-type or from TNF-alpha knockout mice. Six weeks after reconstitution, the chimeric mice were treated with cisplatin and renal structural and functional parameters were measured. Chimeras with kidneys of wild-type animals all developed significant renal failure after 72 h of cisplatin treatment regardless of the immune cell source. Chimeras with kidneys of TNF-alpha knockout mice showed significantly less renal dysfunction (blood urea nitrogen, serum creatinine, and glomerular filtration rate), renal histologic injury, and serum TNF-alpha levels; again regardless of the immune cell source. Urinary excretion of several proinflammatory cytokines was lower in the wild-type bone marrow-knockout kidney chimera mouse than in wild-type background mice. Our results indicate that a substantial portion of circulating and urinary TNF-alpha is derived from nonimmune cells after cisplatin administration. We conclude that the production of TNF-alpha by renal parenchymal cells, rather than by bone marrow-derived infiltrating immune cells, is responsible for cisplatin-induced nephrotoxicity.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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Cisplatin-induced nephrotoxicity is mediated by tumor necrosis factor-α produced by renal parenchymal cells

Zhang

Ramesh

Norbury

et al. 2007

Kidney International

259

188

View full text Add to dashboard Cite

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“…The credibility of these potential mechanisms is presently under investigation. Cellular interactions between monocytes and EC induce early release of proinflammatory cytokines, such as TNF-␣ and IL-1␤ (15,19,30,50). Considering the effects of these cytokines on EC TFA (reference 11 and this study) and the synergistic effect of rIL-1 on TFA of bacterium-infected EC (43), we investigated whether these cytokines mediate TFA induction in our coculture studies.…”

Section: Discussionmentioning

confidence: 99%

Monocytes Augment Bacterial Species- and Strain-Dependent Induction of Tissue Factor Activity in Bacterium-Infected Human Vascular Endothelial Cells

2001

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In bacterial endocarditis (BE), intravascular infection with Staphylococcus aureus, Streptococcus sanguis, orStaphylococcus epidermidis can lead to formation of a fibrin clot on the inner surface of the heart and cause heart dysfunction. The events that start the coagulation in the early stage of the disease are largely unknown. We have recently shown that human endothelial cells (EC) upon binding and internalization of S. aureus, but not S. sanguis or S. epidermidis, express tissue factor (TF)-dependent procoagulant activity (TFA). The present study shows that infection of EC with these three pathogens induces surface expression of intracellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule 1 (VCAM-1) and monocyte adhesion. Subsequent coculture of these cells synergistically enhanced TFA, which was exclusively dependent on TF molecules that were expressed on EC during coculture. TFA induction required direct contact between monocytes and bacterium-infected EC, but the signals for this response were not generated by the binding of monocytes through their ␤ 2 -or ␣ 4 -integrins to ICAM-1 or VCAM-1, respectively, on infected EC. The mechanism by which monocytes induce TFA in bacterium-infected EC was partly mediated by the proinflammatory cytokine interleukin-1 produced by the cells during coculture. Endogenous tumor necrosis factor alpha was not involved. This modulating effect of monocytes on species-and strain-dependent TFA of bacterium-infected EC supports our hypothesis that in an early stage in the pathogenesis of BE, as well as other intravascular infections that lead to detrimental fibrin formation, the coagulation cascade can be activated on the surfaces of EC as a consequence of specific interactions between pathogenic bacteria, EC, and monocytes.

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“…Intrinsic renal cells, including mesangial cells (9 -11) and glomerular (12,13) and tubular epithelial cells (14,15), also have the capacity to produce TNF in vitro. Macrovascular endothelial cells also produce TNF (16,17), but TNF production by glomerular endothelial cells has not been reported. TNF stimulates a variety of proinflammatory responses by intrinsic renal cells.…”

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confidence: 97%

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

106

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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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Naive Monocytes Can Trigger Transendothelial Migration of Peripheral Blood Cells Through the Induction of Endothelial Tumour Necrosis Factor‐α

Cited by 6 publications

References 38 publications

Cisplatin-induced nephrotoxicity is mediated by tumor necrosis factor-α produced by renal parenchymal cells

Cisplatin-induced nephrotoxicity is mediated by tumor necrosis factor-α produced by renal parenchymal cells

Monocytes Augment Bacterial Species- and Strain-Dependent Induction of Tissue Factor Activity in Bacterium-Infected Human Vascular Endothelial Cells

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

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