Effect of immunosuppression on damage, leukocyte infiltration, and regeneration after severe warm ischemia/reperfusion renal injury

Ysebaert, Dirk; Greef, Kathleen E. De; Vercauteren, Sven R.; Verhulst, Anja; Kockx, M.; Verpooten, Gert A.; Broe, Marc E. De

doi:10.1046/j.1523-1755.2003.00150.x

Cited by 48 publications

(37 citation statements)

References 34 publications

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“…As shown in Fig. 2A (11)(12)(13)(14)(15)(16)(17)(18). However, infiltrating leukocytes appear to return to previous basal levels by 24 h after injury.…”

Section: Opn Deficiency Leads To Less Kidney Injurymentioning

confidence: 94%

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Osteopontin Expressed in Tubular Epithelial Cells Regulates NK Cell-Mediated Kidney Ischemia Reperfusion Injury

Zhang

Shek

Wang

et al. 2010

The Journal of Immunology

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Renal ischemia reperfusion injury (IRI) occurs after reduced renal blood flow and is a major cause of acute injury in both native and transplanted kidneys. Studies have shown diverse cell types in both the innate and the adaptive immune systems participate in kidney IRI as dendritic cells, macrophages, neutrophils, B cells, CD4+ NK+ cells, and CD4+ T cells all contribute to this form of injury. Recently, we have found that NK cells induce apoptosis in tubular epithelial cells (TECs) and also contribute to renal IRI. However, the mechanism of NK cell migration and activation during kidney IRI remains unknown. In this study, we have identified that kidney TECs express a high level of osteopontin (OPN) in vitro and in vivo. C57BL/6 OPN-deficient mice have reduced NK cell infiltration with less tissue damage compared with wild-type C57BL/6 mice after ischemia. OPN can directly activate NK cells to mediate TEC apoptotic death and can also regulate chemotaxis of NK cells to TECs. Taken together, our study’s results indicate that OPN expression by TECs is an important factor in initial inflammatory responses that involves NK cells activity in kidney IRI. Inhibiting OPN expression at an early stage of IRI may be protective and preserve kidney function after transplantation.

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“…As shown in Fig. 2A (11)(12)(13)(14)(15)(16)(17)(18). However, infiltrating leukocytes appear to return to previous basal levels by 24 h after injury.…”

Section: Opn Deficiency Leads To Less Kidney Injurymentioning

confidence: 94%

“…+ NK + cells, CD3 2 NK1.1 + cells, and CD4 + T cells that also infiltrate into the kidney shortly after injury (11)(12)(13)(14)(15)(16)(17)(18)(19)(20)(21).…”

mentioning

confidence: 99%

Osteopontin Expressed in Tubular Epithelial Cells Regulates NK Cell-Mediated Kidney Ischemia Reperfusion Injury

Zhang

Shek

Wang

et al. 2010

The Journal of Immunology

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“…Based on the mechanisms mentioned above, the use of immunosuppressive drugs and approaches to inhibit leukocyte adhesion warrant further investigation, and may yield promising renoprotective effects (219,220).…”

Section: Therapeutic Implications and Perspectivesmentioning

confidence: 99%

Renal Hypoxia and Dysoxia After Reperfusion of the Ischemic Kidney

Legrand

Mik

Johannes³

et al. 2008

Mol Med

238

169

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Ischemia is the most common cause of acute renal failure. Ischemic-induced renal tissue hypoxia is thought to be a major component in the development of acute renal failure in promoting the initial tubular damage. Renal oxygenation originates from a balance between oxygen supply and consumption. Recent investigations have provided new insights into alterations in oxygenation pathways in the ischemic kidney. These findings have identified a central role of microvascular dysfunction related to an imbalance between vasoconstrictors and vasodilators, endothelial damage and endothelium-leukocyte interactions, leading to decreased renal oxygen supply. Reduced microcirculatory oxygen supply may be associated with altered cellular oxygen consumption (dysoxia), because of mitochondrial dysfunction and activity of alternative oxygen-consuming pathways. Alterations in oxygen utilization and/or supply might therefore contribute to the occurrence of organ dysfunction. This view places oxygen pathways' alterations as a potential central player in the pathogenesis of acute kidney injury. Both in regulation of oxygen supply and consumption, nitric oxide seems to play a pivotal role. Furthermore, recent studies suggest that, following acute ischemic renal injury, persistent tissue hypoxia contributes to the development of chronic renal dysfunction. Adaptative mechanisms to renal hypoxia may be ineffective in more severe cases and lead to the development of chronic renal failure following ischemia-reperfusion. This paper is aimed at reviewing the current insights into oxygen transport pathways, from oxygen supply to oxygen consumption in the kidney and from the adaptation mechanisms to renal hypoxia. Their role in the development of ischemia-induced renal damage and ischemic acute renal failure are discussed.

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“…They concluded that treatment with CsA signifi cantly increased renal postreperfusion morphologic damage, interstitial leukocytes, and regeneration. 33 Ahmed and colleagues 34,35 studied the effect in Sprague-Dawley rats of a daily injection of 15 mg of cyclosporine on kidneys subjected to 30 minutes of renal warm ischemia. Renal injury and fi brosis were assessed histologically together with immunohistochemistry for collagen III, transforming growth factor (TGF)-beta1, ED1 (macrophage marker), and alphasmooth muscle actin.…”

Section: Interaction Between Cyclosporine and I/r Injury In Experimenmentioning

confidence: 99%

Safety of Cyclosporine in Warm Ischemia Transplanted Kidneys: A Selective Review

Ahmed

2009

Dialysis & Transplantation

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Selective learning (SL), the ability to select items to learn from among other items, engages cognitive control, which is purportedly mediated by the frontal cortex and its circuitry. Using incentive‐based auditory word recall and expository discourse tasks, we studied the efficiency of SL in children ages 6 to 16 years who had sustained severe traumatic brain injury (TBI) at least 1 year earlier. We hypothesized that SL would be compromised by severe TBI. Results indicated that children with severe TBI performed significantly worse than age‐matched typically developing children on word‐ and discourse‐level measures of SL efficiency with no significant group differences in number of items recalled from auditory word lists or declarative facts. We conclude that severe TBI disrupts incentive‐based cognitive control processes, possibly due to involvement of frontal neural networks. Ann Neurol 2004; 56: 847–853

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Effect of immunosuppression on damage, leukocyte infiltration, and regeneration after severe warm ischemia/reperfusion renal injury

Abstract: Immunosuppressive treatment with CsA or MMF affected significantly and in a different manner post-I/R renal morphologic damage, interstitial leukocyte, accumulation and regeneration.

Cited by 48 publications

References 34 publications

Osteopontin Expressed in Tubular Epithelial Cells Regulates NK Cell-Mediated Kidney Ischemia Reperfusion Injury

Osteopontin Expressed in Tubular Epithelial Cells Regulates NK Cell-Mediated Kidney Ischemia Reperfusion Injury

Renal Hypoxia and Dysoxia After Reperfusion of the Ischemic Kidney

Safety of Cyclosporine in Warm Ischemia Transplanted Kidneys: A Selective Review

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