Interleukin 18 (Il-18) Upregulation in Acute Rejection of Kidney Allograft

Střı́ž, Ilja; Krasna, Eliska; Honsová, Eva; Lácha, J; Petříčková, Kateřina; Jaresova, Marcela; Lodererová, Alena; Böhmová, Radka; Slavčev, Antonij; Vı́tko, Štefan

doi:10.1097/00007890-200407271-01492

Cited by 20 publications

(27 citation statements)

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“…Macrophage-derived TNF-α contributes to insulin resistance and development of hepatic steatosis in diet-induced obesity [37] . It was also reported that either IFN-γ or TNF-α up-regulates gene expression or posttranslational processing of IL-18 in several tissue cell types [15,38,39] , indicating that IL-18 may contribute to the development of insulin resistance-related NAFLD via a complex cytokine network of IL-18 and many other cytokines such as TNF-α, IFN-γ and IL-1β.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of hepatic interleukin-18 production by rosiglitazone in a rat model of nonalcoholic fatty liver disease

Wang¹,

Wang²,

Liu³

et al. 2008

WJG

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AIM:To investigate the effects of rosiglitazone (RGZ) on expression of interleukin-18 (IL-18) and caspase-1 in liver of non-alcoholic fatty liver disease (NAFLD) rats. METHODS: Twenty-eight Sprague-Dawley (SD) rats were randomly divided into control, NAFLD, and RGZ treated NAFLD groups. A NAFLD rat model of NAFLD was established by feeding the animals with a high-fat diet for 12 wk. The NAFLD animals were treated with RGZ or vehicle for the last 4 wk (week 9-12) and then sacrificed to obtain liver tissues. Histological changes were analyzed with HE, oil red O and Masson's trichrome staining. Expressions of IL-18 and caspase-1 were detected using immunohistochemical staining and semi-quantitative reverse-transcription polymerase chain reaction (RT-PCR) analysis. RESULTS: The expression levels of both IL-18 and caspase-1 were higher in the liver of NAFLD group than in the control group. Steatosis, inflammation and fibrosis, found in the liver of NAFLD rats, were significantly improved 4 wk after RGZ treatment. The elevated hepatic IL-18 and caspase-1 expressions in NAFLD group were also significantly attenuated after RGZ treatment. CONCLUSION:RGZ treatment can ameliorate increased hepatic IL-18 production and histological changes in liver of NAFLD rats. The beneficial effects of RGZ on NAFLD may be partly due to its inhibitory effect on hepatic IL-18 production.

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Section: Discussionmentioning

confidence: 99%

Inhibition of hepatic interleukin-18 production by rosiglitazone in a rat model of nonalcoholic fatty liver disease

Wang¹,

Wang²,

Liu³

et al. 2008

WJG

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“…There was strong positive immunoreactivity in the proximal tubules of patients with acute rejection. There was also strong immunoreactivity in infiltrating leukocytes and endothelium, suggesting upregulation in the setting of immunopathological reactions (84). In a study of critically ill adult patients with acute respiratory distress syndrome (ARDS), increased urinary IL-18 was found to be an early marker of AKI, preceding changes in serum creatinine by 1−2 days, and was an independent predictor of death (85).…”

Section: Interleukin-18mentioning

confidence: 99%

Biomarkers of Acute Kidney Injury

Vaidya

Ferguson

Bonventre

2008

Annu. Rev. Pharmacol. Toxicol.

631

457

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Acute kidney injury (AKI) is a common condition with a high risk of death. The standard metrics used to define and monitor the progression of AKI, such as serum creatinine and blood urea nitrogen levels, are insensitive, nonspecific, and change significantly only after significant kidney injury and then with a substantial time delay. This delay in diagnosis not only prevents timely patient management decisions, including administration of putative therapeutic agents, but also significantly affects the preclinical evaluation of toxicity thereby allowing potentially nephrotoxic drug candidates to pass the preclinical safety criteria only to be found to be clinically nephrotoxic with great human costs. Studies to establish effective therapies for AKI will be greatly facilitated by two factors: (a) development of sensitive, specific, and reliable biomarkers for early diagnosis/prognosis of AKI in preclinical and clinical studies, and (b) development and validation of high-throughput innovative technologies that allow rapid multiplexed detection of multiple markers at the bedside. Keywordsacute renal failure; clusterin; cystatin-C; cysteine-rich protein-61 (CYR-61); ELISA; ; kidney injury molecule-1 (Kim-1); microfluidics; nanotechnology; neutrophil gelatinaseassociated lipocalin (NGAL) ACUTE KIDNEY INJURY Definition and PrevalenceAcute kidney injury (AKI) is currently recognized as the preferred nomenclature for the clinical disorder formally called acute renal failure (ARF). This transition in terminology served to emphasize that the spectrum of disease is much broader than that subset of patients who experience failure requiring dialysis support (1). This new nomenclature underscores the fact that kidney injury exists along a continuum: The more severe the injury, the more likely the overall outcome will be unfavorable. The Acute Kidney Injury Network (AKIN), which was formed recently in an effort to facilitate improved care of patients who are at risk for AKI, described AKI as "functional or structural abnormalities or markers of kidney damage Copyright © 2008 by Annual Reviews. All rights reserved The Annual Review of Pharmacology and Toxicology is online at http://pharmtox.annualreviews.org DISCLOSURE STATEMENT Dr. Bonventre is a co-inventor on patents involving KIM-1. NIH Public Access Author ManuscriptAnnu Rev Pharmacol Toxicol. Author manuscript; available in PMC 2009 September 11. Published in final edited form as:Annu Rev Pharmacol Toxicol. 2008 ; 48: 463-493. doi:10.1146/annurev.pharmtox.48.113006.094615. NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript including abnormalities in blood, urine, or tissue tests or imaging studies present for less than three months." AKI is associated with the retention of creatinine, urea, and other metabolic waste products that are normally excreted by the kidney. Although severe AKI may result in oliguria or even anuria, urine volume may be normal or even increased (2).Recent epidemiologic data suggest that the progress observed in the un...

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“…A number of acute-phase reactants, such as C-reactive protein (9) and IL-6 (10), have been associated with allograft rejection, although their usefulness also has been disputed (11,12). More recently, monocyte-associated IL-18 has been suggested to be a pertinent biomarker in keeping with growing interest in monocyte infiltration during rejection (see section Other Assays of Peripheral Cell Function) (13).…”

Section: Serum Markers Of Allograft Dysfunctionmentioning

confidence: 99%

Beyond Histology

Mannon¹,

Kirk²

2006

Clinical Journal of the American Society of Nephrology

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Kidney biopsy is the gold standard procedure for the assessment of allograft dysfunction. The differential diagnosis for both acute and chronic dysfunction can encompass a number of different causes, and a biopsy frequently can suggest a specific cause. However, many of these causes are difficult to distinguish on morphologic basis alone, and the information that is obtained from a biopsy is limited with regard to functional and prognostic importance. Additional methods therefore are needed to guide the diagnosis and the treatment of allograft dysfunction, and numerous methods have been studied. Potential markers include protein and gene expression profiles in the peripheral blood, the urine, and the graft itself, all compartments that are relevant to the alloimmune response. Recent comprehensive sequencing of the human genome has led to an unprecedented opportunity to develop these genetic and proteomic techniques, and ongoing evaluations of potential tests have led to an improved understanding of the complexity of immune responses. The future challenge for promising tests is validation in larger patient populations to facilitate their addition to the diagnostic armamentarium.

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Interleukin 18 (Il-18) Upregulation in Acute Rejection of Kidney Allograft

Cited by 20 publications

References 0 publications

Inhibition of hepatic interleukin-18 production by rosiglitazone in a rat model of nonalcoholic fatty liver disease

Inhibition of hepatic interleukin-18 production by rosiglitazone in a rat model of nonalcoholic fatty liver disease

Biomarkers of Acute Kidney Injury

Beyond Histology

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