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

Ouzounidis, Nikolaos; Giakoustidis, Alexandros; Poutahidis, Theofilos; Angelopoulou, Katerina; Iliadis, Stavros; Chatzigiagkos, Antonis; Zacharioudaki, Argyro; Angelopoulos, Stamatios; Papalois, Αpostolos; Papanikolaou, Vasilios; Giakoustidis, Dimitrios

doi:10.1002/lt.24359

Cited by 20 publications

(20 citation statements)

References 41 publications

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“…Monocytes can differentially secrete IL-18 or IL-1β, in response to specific signaling, such as leptin (20). Further, while IL-1β activation is tightly regulated by the inflammasome (19), IL-18 can be activated by non-canonical pathways (caspase-3 and Fas-induced caspase-8) and is regulated by the endogenous inhibitor, IL-18BP (6, 28, 38). Thus, IL-18 may represent a common signal downstream of different inflammatory pathways, and may occasionally function independent of IL-1β activity.…”

Section: Discussionmentioning

confidence: 99%

ASC Methylation and Interleukin-1β Are Associated with Aerobic Capacity in Heart Failure

Butts

Butler

Dunbar

et al. 2017

Medicine &Amp; Science in Sports &Amp; Exercise

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Background Aerobic capacity, as measured by peak oxygen uptake (V̇O2), is one of the most powerful predictors of prognosis in heart failure (HF). Inflammation is a key factor contributing to alterations in aerobic capacity, and interleukin (IL)-1 cytokines are implicated in this process. The adaptor protein ASC is necessary for inflammasome activation of IL-1β and IL-18. ASC expression is controlled through epigenetic modification; lower ASC methylation is associated with worse outcomes in HF. The purpose of this study is to examine the relationships between ASC methylation, IL-1β, and IL-18 with peak V̇O2 in persons with HF. Methods This study examined the relationship between ASC methylation, IL-1β, and IL-18 with peak V̇O2 in 54 stable outpatients with HF. All participants were NYHA class II or III, not engaged in an exercise program, and physically able to complete an exercise treadmill test. Results Mean peak V̇O2 was 16.68 ± 4.7 ml/kg/min. Peak V̇O2was positively associated with mean percent ASC methylation (r=.47, p=.001) and negatively associated with IL-1β (r=-.38, p=.007). Multiple linear regression models demonstrated that peak V̇O2 increased by 2.30 ml/kg/min for every 1% increase in ASC methylation and decreased by 1.91 ml/kg/min for every 1 pg/mL increase in plasma IL-1β. Conclusions Mean percent ASC methylation and plasma IL-1β levels are associated with clinically meaningful differences in peak V̇O2 in persons with HF. Inflammasome activation may play a mechanistic role in determining aerobic capacity. ASC methylation is a potentially modifiable mechanism for reducing the inflammatory response, thereby improving aerobic capacity in HF.

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Section: Discussionmentioning

confidence: 99%

ASC Methylation and Interleukin-1β Are Associated with Aerobic Capacity in Heart Failure

Butts

Butler

Dunbar

et al. 2017

Medicine &Amp; Science in Sports &Amp; Exercise

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“…The total tumor area per total liver area ratio was also calculated for each mouse liver section. IHC-positive cells or pixels were counted in hepatocellular adenoma images of x20 representative high power fields and results were recorded as number of cells or pixels per image as previously described (25). The ImageJ image processing and analysis program (National Institutes of Health, Bethesda, MD, USA) was used for all histomorphometrical assessments.…”

Section: Methodsmentioning

confidence: 99%

Effects of Wnt‑1 blockade in DEN‑induced hepatocellular adenomas of mice

et al. 2017

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Abstract. Recent evidence has suggested that downregulation of the Wnt/β-catenin signaling pathway may contribute to the development and growth of HCC. Consequently, elements of this pathway have begun to emerge as potential targets for improving outcomes of anti-HCC. Thus, the present study sought to examine the effects of Wnt-1 blockade using the classical diethylnitrosamine (DEN)-induced chemical carcinogenesis mouse model of HCC. The depletion of Wnt-1 using neutralizing antisera was done for ten consecutive days at the age of 9 months and mice were examined for the following 20 days. At that time, DEN-treated mice had multiple variably-sized hepatic cell adenomas. Anti-Wnt-1 was particularly potent in suppressing the expression of critical elements of the Wnt/β-catenin signaling pathway, such as β-catenin and Frizzled-1 receptor, however, not Dickkopf-related protein 1. This effect co-existed with the suppression of Cyclin D1, FOXM1, NF-κΒ and c-Jun commensurate with proliferation and apoptosis blockade in hepatocellular adenomas, and reduced Bcl-2 and c-Met in the serum of mice. Nonetheless, tumor size and multiplicity were found to be unaffected, suggesting that apoptosis may be equally important to proliferation in the context of counteracting DEN induced hepatocellular adenomas of mice.

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“…Initial IR-induced hepatic injury is reported to be mediated by activated Kupffer cells without dependence on neutrophils[77,78]. The later phase of IR injury is dependent upon hepatic neutrophil sequestration, and the subsequent increased adherence between neutrophils and endothelial cells.…”

Section: Mip-2 Production In Murine Models Of Acute Liver Injurymentioning

confidence: 99%

Macrophage inflammatory protein-2 as mediator of inflammation in acute liver injury

Qin

Liu

et al. 2017

WJG

110

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Macrophage inflammatory protein (MIP)-2 is one of the CXC chemokines and is also known as chemokine CXC ligand (CXCL2). MIP-2 affects neutrophil recruitment and activation through the p38 mitogen-activated-protein-kinase-dependent signaling pathway, by binding to its specific receptors, CXCR1 and CXCR2. MIP-2 is produced by a variety of cell types, such as macrophages, monocytes, epithelial cells, and hepatocytes, in response to infection or injury. In liver injury, activated Kupffer cells are known as the major source of MIP-2. MIP-2-recruited and activated neutrophils can accelerate liver inflammation by releasing various inflammatory mediators. Here, we give a brief introduction to the basic molecular and cellular sources of MIP-2, and focus on its physiological and pathological functions in acute liver injury induced by concanavalin A, lipopolysaccharides, irradiation, ischemia/reperfusion, alcohol, and hypoxia, and hepatectomy-induced liver regeneration and tumor colorectal metastasis. Further understanding of the regulatory mechanisms of MIP-2 secretion and activation may be helpful to develop MIP-2-targeted therapeutic strategies to prevent liver inflammation.

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

Cited by 20 publications

References 41 publications

ASC Methylation and Interleukin-1β Are Associated with Aerobic Capacity in Heart Failure

ASC Methylation and Interleukin-1β Are Associated with Aerobic Capacity in Heart Failure

Effects of Wnt‑1 blockade in DEN‑induced hepatocellular adenomas of mice

Macrophage inflammatory protein-2 as mediator of inflammation in acute liver injury

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