T cells as mediators in renal ischemia/reperfusion injury

Ysebaert, Dirk; Greef, Kathleen E. De; Beuf, Annelies De; Rompay, An R. Van; Vercauteren, Sven R.; Persy, Veerle P.; Broe, Marc E. De

doi:10.1111/j.1523-1755.2004.761_4.x

Cited by 180 publications

(149 citation statements)

References 38 publications

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“…Tissue injury after ischemia was not only caused by hypoxia from interrupted blood supply but also the activated inflammatory response by reperfusion. The peripheral leukocytes recruit and the interstitial cells proliferated in the target tissue (Ysebaert et al, 2004). An innate immune system was found to be important for the pathogenesis of IRI in recent years.…”

Section: Discussionmentioning

confidence: 99%

Protective effect of indomethacin in renal ischemia-reperfusion injury in mice

Zhu

Zhou

Jiang

et al. 2014

J. Zhejiang Univ. Sci. B

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Abstract:Objective: To evaluate the renoprotection effects of non-steroidal anti-inflammatory drugs (NSAIDs) in renal ischemia-reperfusion injury (IRI) and the cyclooxygenase (COX)-1/2 blockade association by indomethacin (IMT) in the mice model. Methods: After the left renal pedicle of mice was clamped, IMT was administrated by intraperitoneal injection with four doses: 1, 3, 5, and 7 mg/kg. Blood and kidney samples were collected 24 h after IRI. The renal functions were assayed by the cytokines and serum creatinine (SCr) using enzyme-linked immunosorbent assay (ELISA) kits. Kidney samples were analyzed by hematoxylin and eosin (H&E) and immunohistochemistry stainings. Results: The mice administered with 5 mg/kg IMT had a marked reduction in SCr and significantly less tubular damage. The tumor necrosis factor α (TNF-α) activity in renal homogenates and interleukin 6 (IL-6) activity in serum had a marked reduction at doses of 5 and 7 mg/kg IMT. The administration of 3 and 5 mg/kg IMT had a marked reduction in the ratio of thromboxane B2 to 6-keto-prostaglandin F 1α . COX-1 and COX-2 stainings were weaker in 5 mg/kg IMT groups than that in the other groups. Conclusions: There was a dose response in the IMT function of renal IRI in mice, and IMT had a protective effect in a certain dose range. The effect of IMT on mice IRI was related to COX-1/2 blockades.

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Section: Discussionmentioning

confidence: 99%

Protective effect of indomethacin in renal ischemia-reperfusion injury in mice

Zhu

Zhou

Jiang

et al. 2014

J. Zhejiang Univ. Sci. B

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“…This discrepancy may be a consequence of the different route of administration, or the strain of rats used, among other possible factors. In general, infiltrating cells appearing after ATN are believed to play a relevant role in the local delivery of cytokines, and they are known to appear rapidly after injury and disappear upon complete repair (Ghielli et al, 1996;Ysebaert et al, 2004).…”

Section: Histopathologymentioning

confidence: 99%

Clinicopathological and Tissue Indicators of Para-Aminophenol Nephrotoxicity in Sprague–Dawley Rats

Yang¹,

Trajkovic

Illanes³

et al. 2007

Toxicol Pathol

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A model of para-aminophenol (PAP) nephrotoxicity in Sprague-Dawley rats was utilized to characterize potential indicators of toxicity in the kidney and in biofluids, and to chronicle the progression of acute renal injury. Rats were administered PAP at a low or high dose and examined terminally at 6, 24 and 48 hours (4 animals/group with matching controls). Acute tubular necrosis was observed in the medullary rays (low and high doses) and the outer stripe of outer medulla (high dose only) as early as 6 hours postdosing. Starting at 24 hours, regeneration of the tubular epithelium was evident in both low and high dose studies. Associated with the tubular lesions, we observed elevation of urinary α-glutathione S-transferase levels, an indicator of proximal tubular injury. By immunohistochemistry of the kidney, decreased γ -glutamylcysteine synthetase expression correlated with tubular injury, especially at high dose, whereas elevation of vimentin, osteopontin, and Ki-67 expression was concurrent with tubular regeneration. Clusterin and kidney injury molecule-1 displayed expression patterns characteristic of both renal injury and regeneration. Taken together, this study provided insight into the progression of nephrotoxicity, and allowed the evaluation of potential urinary and tissue protein biomarkers that could complement the early detection of acute tubular injury.

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“…1 Animal models of ischemia/ reperfusion (I/R), where the inflammatory re-sponse can be more carefully studied, show that ischemic injury is accompanied by the rapid influx of polymorphonuclear leukocytes, lymphocytes, and macrophages into the interstitium. [2][3][4] These cells are believed to home to the injured kidney in response to inflammatory cytokines such as monocyte chemoattractant protein-1, stromal cell-derived factor-1, IL-6 and IL-8/keratinocyte chemoattractant produced locally by cells such as the resident dendritic cell and injured tubular and endothelial cells. 5,6 In the early phase of renal I/R injury, leukocyte populations seem to be detrimental because they promote apoptotic cell death by releasing reactive oxygen species and activating caspases.…”

mentioning

confidence: 99%

Distinct Macrophage Phenotypes Contribute to Kidney Injury and Repair

Lee¹,

Huen²,

Nishio³

et al. 2011

Journal of the American Society of Nephrology

745

796

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The ischemically injured kidney undergoes tubular cell necrosis and apoptosis, accompanied by an interstitial inflammatory cell infiltrate. In this study, we show that iNos-positive proinflammatory (M1) macrophages are recruited into the kidney in the first 48 hours after ischemia/reperfusion injury, whereas arginase 1-and mannose receptor-positive, noninflammatory (M2) macrophages predominate at later time points. Furthermore, depletion of macrophages before ischemia/reperfusion diminishes kidney injury, whereas depletion at 3 to 5 days after injury slows tubular cell proliferation and repair. Infusion of Ifn␥-stimulated, bone marrowderived macrophages into macrophage-depleted mice at the time of kidney reperfusion restored injury to the level seen without macrophage depletion, suggesting that proinflammatory macrophages worsen kidney damage. In contrast, the appearance of macrophages with the M2 phenotype correlated with the proliferative phase of kidney repair. In vitro studies showed that IFN␥-stimulated, proinflammatory macrophages begin to express markers of M2 macrophages when cocultured with renal tubular cells. Moreover, IL-4 -stimulated macrophages with an M2 phenotype, but not IFN␥-stimulated proinflammatory macrophages, promoted renal tubular cell proliferation. Finally, tracking fluorescently labeled, IFN␥-stimulated macrophages that were injected after injury showed that inflammatory macrophages can switch to an M2 phenotype in the kidney at the onset of kidney repair. Taken together, these studies show that macrophages undergo a switch from a proinflammatory to a trophic phenotype that supports the transition from tubule injury to tubule repair.

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T cells as mediators in renal ischemia/reperfusion injury

Cited by 180 publications

References 38 publications

Protective effect of indomethacin in renal ischemia-reperfusion injury in mice

Protective effect of indomethacin in renal ischemia-reperfusion injury in mice

Clinicopathological and Tissue Indicators of Para-Aminophenol Nephrotoxicity in Sprague–Dawley Rats

Distinct Macrophage Phenotypes Contribute to Kidney Injury and Repair

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