Postischemic reperfusion injury and allograft arteriosclerosis

Fellström, Bengt; Akuyrek, Levent M; Backman, U.; Larsson, Erik; Melin, Jonas; Zezina, Lilija

doi:10.1016/s0041-1345(98)01412-2

Cited by 46 publications

(26 citation statements)

References 29 publications

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“…This remains a significant problem in surgical procedures, and is a limitation of liver transplantation [25][26][27]. Hepatic I/R causes functional and structural damage to liver cells.…”

Section: Discussionmentioning

confidence: 99%

Triptolide protects mice from ischemia/reperfusion injury by inhibition of IL-17 production

Xia

Wang

et al. 2011

International Immunopharmacology

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“…This remains a significant problem in surgical procedures, and is a limitation of liver transplantation [25][26][27]. Hepatic I/R causes functional and structural damage to liver cells.…”

Section: Discussionmentioning

confidence: 99%

Triptolide protects mice from ischemia/reperfusion injury by inhibition of IL-17 production

Xia

Wang

et al. 2011

International Immunopharmacology

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“…Indeed, IRI, an Ag-independent component of the harvesting insult represents a serious problem affecting transplantation outcome as it causes up to 10% of early organ failure, and increases the risk of both acute and chronic rejection (3,4). Additionally, because of the higher susceptibility of marginal livers to ischemia, IRI contributes to the acute shortage of livers available for transplantation.…”

Section: Schemia-reperfusion (Ir)mentioning

confidence: 99%

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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“…This can lead to postoperative organ insufficiency. Ischemia reperfusion injury is also associated with chronic rejection due to arteriosclerosis [12] caused by IRI. IRI results in adipocutaneous and musculoskeletal flap necrosis as well as nonfunctioning microvascular flaps.…”

Section: Introductionmentioning

confidence: 99%

Remote Ischemic Preconditioning: A Novel Protective Method From Ischemia Reperfusion Injury—A Review

Tapuria

Kumar

Habib

et al. 2008

Journal of Surgical Research

304

225

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Postischemic reperfusion injury and allograft arteriosclerosis

Cited by 46 publications

References 29 publications

Triptolide protects mice from ischemia/reperfusion injury by inhibition of IL-17 production

Triptolide protects mice from ischemia/reperfusion injury by inhibition of IL-17 production

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

Remote Ischemic Preconditioning: A Novel Protective Method From Ischemia Reperfusion Injury—A Review

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