Attenuation of myocardial injury by HMGB1 blockade during ischemia/reperfusion is toll-like receptor 2-dependent.

Genetic or pharmacological ablation of toll-like receptor 2 (TLR2) protects against myocardial ischemia/reperfusion injury (MI/R). However, the endogenous ligand responsible for TLR2 activation has not yet been detected. The objective of this study was to identify HMGB1 as an activator of TLR2 signalling during MI/R.

Cecum ligation and dissection: a novel modified mouse sepsis model.

Background: The fact that many sepsis therapeutics failed to be translated into the human indicates that there is still a serious need to reassess our models of sepsis research. We aimed to develop a novel modified model of sepsis in the mouse, which simulates the clinical situation more accurately.

Materials And Methods: Sepsis was induced in C57Bl/6 mice by dissecting the cecum and placing the discontinued organ back into the abdomen (cecum ligation and dissection [CLD]).

The fibrinopeptide bβ15-42 reduces inflammation in mice subjected to polymicrobial sepsis.

Sepsis is still a leading cause of death on intensive care units. Despite intensive research, only few new therapies have been developed and used in the clinical setting. The fibrin fragment Bβ15-42 was already shown to preserve endothelial barrier function by binding to VE-cadherin and thus stabilize the interendothelial junctions.

Akt or phosphoinositide-3-kinase inhibition reverses cardio-protection in Toll-like receptor 2 deficient mice.

Aim: Absence or inhibition of Toll-like receptor 2 (TLR2) signalling during murine myocardial ischaemia/reperfusion (MI/R) decreases myocardial necrosis and inflammation, thereby ameliorating cardiac dysfunction and improving survival. In the present study, we provide evidence for the involvement of the phosphoinositide-3-kinase/Akt pathway in TLR2-dependent reperfusion injury.

Methods: Adult male wild-type (WT) and TLR2(-/-) mice were subjected to myocardial ischaemia (30min) and reperfusion (4h).

Measure for measure-determination of infarct size in murine models of myocardial ischemia and reperfusion: a systematic review.

Myocardial ischemia/reperfusion injury (MI/R) is one of the most prominent topics of contemporary research. The frequent failure of potential therapeutic drugs and interventions to transfer to clinical practice demonstrates the limitations in using experimental animal models. Because a variety of transgenic animals are readily available in mice, researchers in recent years have made use of murine models rather than of larger animal models for experimental MI/R.

Left ventricular dilation in toll-like receptor 2 deficient mice after myocardial ischemia/reperfusion through defective scar formation.

Restoration of myocardial blood flow after ischemia triggers an inflammatory response involving toll-like receptors (TLRs). TLR2(-/-)-mice show short-term advantages upon reperfusion injury as compared with WT controls. Accordingly, it has been shown that transient TLR2-blockade prior to reperfusion is associated with improved left-ventricular performance after myocardial scar formation.