Interleukin 1 and Tumor Necrosis Factor Production as the Initial Stimulants of Liver Ischemia and Reperfusion Injury

Suzuki, Shohachi; Toledo‐Pereyra, Luis H.

doi:10.1006/jsre.1994.1140

Cited by 146 publications

(82 citation statements)

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“…Increased TNF-␣ and IL-1 plasma levels were observed as early as 5 min of liver reperfusion (17). Their functional role was confirmed by neutralization experiments in which IL-1 or TNF-␣ blockade ameliorated the severity of IRI (18,19).…”

Section: Discussionmentioning

confidence: 74%

CXCR3+CD4+ T Cells Mediate Innate Immune Function in the Pathophysiology of Liver Ischemia/Reperfusion Injury

Zhai

Shen

Hancock

et al. 2006

The Journal of Immunology

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Ischemia-reperfusion injury (IRI), an innate immune-dominated inflammatory response, develops in the absence of exogenous Ags. The recently highlighted role of T cells in IRI raises a question as to how T lymphocytes interact with the innate immune system and function with no Ag stimulation. This study dissected the mechanism of innate immune-induced T cell recruitment and activation in rat syngeneic orthotopic liver transplantation (OLT) model. Liver IRI was induced after cold storage (24–36 h) at 4°C in University of Wisconsin solution. Gene products contributing to IRI were identified by cDNA microarray at 4-h posttransplant. IRI triggered increased intrahepatic expression of CXCL10, along with CXCL9 and 11. The significance of CXCR3 ligand induction was documented by the ability of neutralizing anti-CXCR3 Ab treatment to ameliorate hepatocellular damage and improve 14-day survival of 30-h cold-stored OLTs (95 vs 40% in controls; p < 0.01). Immunohistology analysis confirmed reduced CXCR3+ and CD4+ T cell infiltration in OLTs after treatment. Interestingly, anti-CXCR3 Ab did not suppress innate immune activation in the liver, as evidenced by increased levels of IL-1β, IL-6, inducible NO synthase, and multiple neutrophil/monokine-targeted chemokine programs. In conclusion, this study demonstrates a novel mechanism of T cell recruitment and function in the absence of exogenous Ag stimulation. By documenting that the execution of innate immune function requires CXCR3+CD4+ T cells, it highlights the critical role of CXCR3 chemokine biology for the continuum of innate to adaptive immunity in the pathophysiology of liver IRI.

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Section: Discussionmentioning

confidence: 74%

CXCR3+CD4+ T Cells Mediate Innate Immune Function in the Pathophysiology of Liver Ischemia/Reperfusion Injury

Zhai

Shen

Hancock

et al. 2006

The Journal of Immunology

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“…Several mechanisms have been considered to explain I/R injury of the liver. Activation of KC with enhanced formation of ROS and secretion of inflammatory cytokines and proteolytic enzymes are considered to play an important role in liver reperfusion injury [28,29] . Additionally, migration of activated polymorphonuclear leukocytes at the injury site may prolong the injury as a result of the production of inflammatory cytokines, adhesion molecules, and ROS [30,31] .…”

Section: Discussionmentioning

confidence: 99%

Resveratrol attenuates oxidative stress and histological alterations induced by liver ischemia/reperfusion in rats

Gedik¹,

Gırgın²,

Öztürk³

et al. 2008

WJG

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AIM:To investigate the effects of resveratrol on liver ischemia/reperfusion (I/R) injury in rats. METHODS: A total of 40 male Sprague-Dawley rats weighing 240-290 g were randomized into four groups of ten: (1) controls: data from unmanipulated animals; (2) sham group: rats subjected to the surgical procedure, except for liver I/R, and given saline; (3) I/R group: rats underwent liver ischemia for 45 min followed by reperfusion for 45 min; (4) I-R/Resveratrol group: rats pretreated with resveratrol (10 µmol/L, iv). Liver tissues were obtained to determine antioxidant enzyme levels and for biochemical and histological evaluation. RESULTS: Plasma aminotransferase activities were higher in the I/R group than in the I-R/Resveratrol group. Malondialdehyde levels and the hepatic injury score decreased, while superoxide dismutase, catalase, and glutathione peroxidase levels increased in group 4 compared to group 3. In group 4, histopathological changes were significantly attenuated in resveratroltreated livers. CONCLUSION: These results suggest that resveratrol has protective effects against hepatic I/R injury, and is a potential therapeutic drug for ischemia reperfusionrelated liver injury.

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“…It has been well documented that TNF-α is an important mediator of inflammation, mediating the spread and development of the immune reaction from a central site, which is a key factor in hepatic I/R injury (Scales et al, 1994;Suzuki and Toledo-Pereyra, 1994;Imanishi et al, 1997). The pathological processes that mediate liver I/R injury include center granulocyte aggregation, protein enzyme leakage, and hepatocyte necrosis (Imanishi et al, 1997); however, the role of TNF-α in hepatic I/R injury is still not completely determined.…”

Section: Introductionmentioning

confidence: 99%

Inhibition of gap junctions relieves the hepatotoxicity of TNF-α

Chen¹,

Wang²,

Huang³

et al. 2015

Genet. Mol. Res.

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ABSTRACT. The aim of this study was to observe the influence of gap junction (GJ) functional changes on the hepatotoxicity of TNF-α. Three different methods were employed to study functional effects of the GJ inhibition: 1) pretreatment with a GJ inhibitor; 2) inoculation of cells at high and low densities; and 3) inhibition of the expression of connexin 32 (Cx32) by small inhibitory RNA transfection. We then observed the influence of these treatments on hepatotoxicity following treatment with different concentrations of TNF-α for various duration. The hepatotoxicity of TNF-α was observed to occur in a dose-and timedependent manner; after pretreatment inhibition, the hepatotoxicity of TNF-α was significantly reduced (P < 0.01). The hepatotoxicity of TNF-α was also found to be remarkably lower in cells that had been inoculated at low density (as measured by the amount of GJ formation among cells) than in those inoculated at density (P < 0.01). In addition, following Cx32 inhibition, the hepatotoxicity of TNF-α was significantly decreased (P < 0.01) as well. Together, these results suggest that inhibition of GJ function or of its component Cx32 significantly 11897Gap junctions in the hepatotoxicity of TNF-α ©FUNPEC-RP www.funpecrp.com.br Genetics and Molecular Research 14 (4): 11896-11904 (2015) decreases the hepatotoxicity of TNF-α, and that the expression of Cx32 plays an important role in the hepatotoxicity of TNF-α.

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Interleukin 1 and Tumor Necrosis Factor Production as the Initial Stimulants of Liver Ischemia and Reperfusion Injury

Cited by 146 publications

References 0 publications

CXCR3+CD4+ T Cells Mediate Innate Immune Function in the Pathophysiology of Liver Ischemia/Reperfusion Injury

CXCR3+CD4+ T Cells Mediate Innate Immune Function in the Pathophysiology of Liver Ischemia/Reperfusion Injury

Resveratrol attenuates oxidative stress and histological alterations induced by liver ischemia/reperfusion in rats

Inhibition of gap junctions relieves the hepatotoxicity of TNF-α

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