Effect of IL-18 binding protein on hepatic ischemia-reperfusion injury induced by infrarenal aortic occlusion

Özsoy, Mustafa; Gönül, Yücel; Bal, Ahmet; Özkeçeci, Ziya Taner; Celep, Rüçhan Bahadır; Adalı, Fahri; Hazman, Ömer; Koçak, Ahmet; Tosun, Murat

doi:10.4174/astr.2015.88.2.92

Cited by 21 publications

(17 citation statements)

References 26 publications

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“…Overall, our results add value to recent findings in rats that show the efficacy of IL 18Bp in attenuating both liver and renal ischemic injury by down‐regulating critical proinflammatory cytokines, inflammatory cell infiltration, oxidative stress, and apoptosis.…”

Section: Discussionsupporting

confidence: 81%

Interleukin 18 binding protein ameliorates ischemia/reperfusion–induced hepatic injury in mice

et al. 2016

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Inflammation-associated oxidative stress contributes to hepatic ischemia/reperfusion injury (IRI). Detrimental inflammatory event cascades largely depend on activated Kupffer cells (KCs) and neutrophils, as well as proinflammatory cytokines, including tumor necrosis factor α (TNF-α) and interleukin (IL) 18. The aim of our study was to evaluate the effects of IL 18 binding protein (IL 18Bp) in hepatic IRI of mice. Thirty C57BL/6 mice were allocated into 3 groups: sham operation, ischemia/reperfusion (I/R), and I/R with intravenous administration of IL 18Bp. Hepatic ischemia was induced for 30 minutes by Pringle's maneuver. After 120 minutes of reperfusion, mice were euthanized, and the liver and blood samples were collected for histological, immunohistochemical, molecular, and biochemical analyses. I/R injury induced the typical liver pathology and upregulated IL-18 expression in the liver of mice. Binding of IL 18 with IL 18Bp significantly reduced the histopathological indices of I/R liver injury and KC apoptosis. The I/R-induced increase of TNF-α, malondialdehyde, aspartate aminotransferase, and alanine aminotransferase levels was prevented in statistically significant levels because of the pretreatment with IL 18Bp. Likewise, blocking of IL 18 ablated the I/R-associated elevation of nuclear factor kappa B, c-Jun, myeloperoxidase, and IL 32 and the up-regulation of neutrophils and T-helper lymphocytes. Administration of IL 18Bp protects the mice liver from I/R injury by intervening in critical inflammation-associated pathways and KC apoptosis.

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Section: Discussionsupporting

confidence: 81%

Interleukin 18 binding protein ameliorates ischemia/reperfusion–induced hepatic injury in mice

et al. 2016

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“…Administration of IL-18BP mitigated hepatic oxidative stress, which was well-recognized to trigger production of pro-inflammatory cytokines and cell adhesion molecules. Afterwards, hepatic pathological structure was protected [8].…”

Section: Role Of Il-18 In Liver Ischemia-reperfusion Injurymentioning

confidence: 99%

“…Other non-immune cells can also express IL-18 such as intestinal and airway epithelial cells, keratinocytes, airway epithelium, corneal epithelial cells, renal tubular epithelial cells [7]. The main role of IL-18 is to crucially stimulate lymphocytes to produce the IFN-␥ [5] a equal contribution and regulate macrophages activity, thereby increasing the expression of pro-inflammatory cytokines including IL-6, IL-1␤, CCL4 (macrophage inflammatory protein-1 ␤), CXCL2 (macrophage inflammatory protein-2), and CCL2 (monocyte chemotactic protein-1) [8]. IL-18 in conjunction with IL-12 can stimulate the production of IFN-␥ by B and T cells and potentiate the cytolytic activity of natural killer (NK) cells, and induce Th1 and Th2 responses (figure 1) [9,10].…”

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confidence: 99%

Role of IL-18 in transplant biology

Liu

Chen

Liu

et al. 2018

European Cytokine Network

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Since pro-inflammatory cytokine IL-18 and its receptor (IL-18R) are closely involved in regulating both adaptive and innate immune responses, it is conceivable that they might play an important role in organ transplantation. IL-18 can stimulate lymphocytes to produce the IFN-␥ and regulate macrophage activity, thereby increasing the expression of proinflammatory cytokines including IL-1␤, IL-6, CCL4 (macrophage inflammatory protein-1 ␤), CXCL2 (macrophage inflammatory protein-2), and CCL2 (monocyte chemotactic protein-1). Nevertheless, the IL-18 signaling pathway and its underlying mechanisms remain obscure in transplant biology. This review is to summarize recent advances in our knowledge about the IL-18 signaling pathway and to analyze their functions in transplant-related biology. It was found that IL-18/IL-18R signaling pathway contributed to vascular transplantation, ischemmia/reperfusion, acute kidney injury, and acute rejection of kidney/liver/heart transplantation. IL-18 was a potential CYP3A expression modulator and was capable of affecting tacrolimus pharmacokinetics. Neutralizing IL-18 by its inhibitor IL-18 binding protein could efficiently suppress the production of injury-associated cytokines such as IL-6, TNF-␣, IFN-␥, CXCL10 (IFN-␥-inducible protein10), and CX 3 CL1 (fractalkine) and improve allograft function. Blockade of IL-18 signaling could regulate cardiomyocyte apoptosis and inhibit Th17 cells differentiation. Alteration of IL-18 levels was suggested as a biomarker for predicting ongoing allograft outcome. All these activities could deepen our understanding of immunobiological role of IL-18 and its receptor in the field of organ transplantation. Intervention of IL-18 signaling pathway might be utilized as a therapeutic strategy in clinic.

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“…Surgical procedure is known to stimulate a series of hormonal, metabolic and inflammatory changes that together form stress response [ 6 ]. Under stress response, sympathetic-adrenal medullary system is stimulated and serum catecholamine level increases.…”

Section: Discussionmentioning

confidence: 99%

Analgesic efficacy of bilateral superficial and deep cervical plexus block in patients with secondary hyperparathyroidism due to chronic renal failure

Su¹,

Zhang²,

Zhang³

et al. 2015

Ann Surg Treat Res

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PurposeSecondary hyperparathyroidism (SHPT) develops in patients with chronic renal failure. This study aimed to compare analgesic efficacy in SHPT patients who undergo subtotal parathyroidectomy after superficial versus deep cervical plexus block.MethodsSixty chronic renal failure patients with SPHT scheduled for subtotal parathyroidectomy were randomized to receive general anesthesia (group GA), general anesthesia plus bilateral superficial and deep cervical plexus block (group BD), or general anesthesia plus bilateral superficial cervical plexus block (group BS) (n = 20). Bilateral superficial cervical plexus block or combined superficial and deep cervical plexus block with 0.5% ropivacaine was administered. Postoperative pain was assessed using visual analogue scale (VAS).ResultsVAS score at 1 hour, 4 hours, and 8 hours after operation was 3.71 ± 0.60, 2.72 ± 0.54, 2.17 ± 0.75 in BS group; 4.00 ± 0.28, 2.89 ± 0.21, and 2.46 ± 1.01 in BD group, significantly lower than in GA group (6.50 ± 0.50, 5.02 ± 0.54, and 4.86 ± 0.51, respectively). The dosage of tramadol was 109.0 ± 35.2 mg in BS group and 93.0 ± 24.52 mg in BD group, significantly lower than in GA group (300.0 ± 27.13 mg). The incidence of complications in GA group (90%) was significantly higher than in BS group (30%) and BD group (15%). Serum glucose and norepinephrine levels were significantly higher at 1 hour, 4 hours, and 8 hours after operation, but returned to baseline levels at 24 hours after operation.ConclusionSuperficial cervical plexus block or combined superficial and deep cervical plexus block effectively reduces postoperative pain, stress response, and complications in SHPT patients who undergo subtotal parathyroidectomy.

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Effect of IL-18 binding protein on hepatic ischemia-reperfusion injury induced by infrarenal aortic occlusion

Cited by 21 publications

References 26 publications

Interleukin 18 binding protein ameliorates ischemia/reperfusion–induced hepatic injury in mice

Interleukin 18 binding protein ameliorates ischemia/reperfusion–induced hepatic injury in mice

Role of IL-18 in transplant biology

Analgesic efficacy of bilateral superficial and deep cervical plexus block in patients with secondary hyperparathyroidism due to chronic renal failure

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