Ischemia-reperfusion injury (IRI) is one of the major causes of acute kidney injury (AKI) and evidence supporting the involvement of both innate and adaptive immunity in renal IRI has accumulated in recent years. In addition to leukocytes, kidney endothelial cells promote inflammation after IRI by increasing adhesion molecule expression and vascular permeability. Kidney tubular epithelial cells...

Complement is implicated in the pathogenesis of ischemia-reperfusion injury (IRI). The activation pathway(s) and effector(s) of complement in IRI may be organ specific and remain to be fully characterized. We previously developed a renal IRI model in decay-accelerating factor (DAF) and CD59 double-knockout (DAF(-/-)CD59(-/-)) mice. In this study, we used this model to dissect the pathway(s) by ...

Background Oxidative stress (OS), the production of free oxygen radicals caused by for instance renal ischemia/reperfusion injury (IRI), results in age associated diseases and accelerated aging. We have shown that preoperative fasting in young-lean C57BL6 male mice protects against renal IRI [1]. Since human patients are usually older and suffer from (co)morbidities, we investigated the effects...

Reperfusion after a period of ischemia results in reperfusion injury (IRI) which involves activation of the inflammatory cascade. In cardiac IRI, IgM natural antibodies (NAb) play a prominent role through binding to altered neoepitopes expressed on damaged cells. Beta 2 Glycoprotein I (β2GPI) is a plasma protein that binds to neoepitopes on damaged cells including anionic phospholipids through ...

Background: The widely adopted Jablonski scoring system for reporting histological damage in kidney ischaemia reperfusion injury (IRI) provides a limited score documenting the degree of necrosis within tubular cells. IRI is a complex process that involves damage to various cellular components of the renal cortex and therefore there is a need to develop a more detailed scoring system. The aims o...

BACKGROUND. Orthotopic liver transplant (OLT) is the primary therapy for end-stage liver disease and acute liver failure. However, ischemia/reperfusion injury (IRI) can severely compromise allograft survival. To understand the evolution of immune responses underlying OLT-IRI, we evaluated longitudinal cytokine expression profiles from adult OLT recipients before transplant through 1 month after...

Reductions in renal microvasculature density and increased lymphocyte activity may play critical roles in the progression of chronic kidney disease (CKD) following acute kidney injury (AKI) induced by ischemia/reperfusion injury (IRI). Vitamin D deficiency is associated with tubulointerstitial damage and fibrosis progression following IRI-AKI We evaluated the effect of vitamin D deficiency in s...

Abstract Coronary heart disease leading to myocardial ischemia is a major cause of failure. A hallmark failure fibrosis. Using murine model ischemia/reperfusion injury (IRI), we showed that, following IRI, in mice genetically deficient the central factor complement system, C3, necrosis was reduced compared with WT mice. Four weeks after ischemic period, C3 −/−mice had significantly less cardiac...

BACKGROUND Although lung transplantation from donation after cardiac death (DCD), especially uncontrolled DCD, is limited by warm ischemic periods, the molecular mechanism of warm ischemia-reperfusion-injury (IRI) has not been well elucidated. The purpose of this study was to clarify the particular longitudinal mechanisms of molecular factors involved in warm IRI. METHODS Cold ischemic-time (...

The complement system is an essential component of innate immunity and plays a major role in the pathogenesis of ischemia-reperfusion injury (IRI). In this study, we investigated the impact of human C1-inhibitor (C1INH) on the early inflammatory response to IRI and the subsequent progression to fibrosis in mice. We evaluated structural damage, renal function, acute inflammatory response, progre...