Mediators of inflammation
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Mediators of inflammation · Jan 2010
Relevance of serum leptin and leptin-receptor concentrations in critically ill patients.
The adipocyte-derived cytokine leptin was implicated to link inflammation and metabolic alterations. We investigated the potential role of leptin components in critically ill patients, because systemic inflammation, insulin resistance, and hyperglycemia are common features of critical illness. Upon admission to Medical Intensive Care Unit (ICU), free leptin and soluble leptin-receptor serum concentrations were determined in 137 critically ill patients (95 with sepsis, 42 without sepsis) and 26 healthy controls. ⋯ However, serum leptin was closely associated with obesity and diabetes and clearly correlated with markers of metabolism and liver function. Leptin-receptor was an unfavourable prognostic indicator, associated with mortality during three years follow-up. Our study indicates a functional role of leptin in the pathogenesis of severe illness and emphasizes the impact of complex metabolic alterations on the clinical outcome of critically ill patients.
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Mediators of inflammation · Jan 2010
Disruption of Nrf2 enhances the upregulation of nuclear factor-kappaB activity, tumor necrosis factor-α, and matrix metalloproteinase-9 after spinal cord injury in mice.
Matrix metalloproteinase-9 (MMP-9) plays an important role in the acute periods of spinal cord injury (SCI), and its expression is related to the inflammation which could cause the disruption of the blood-spinal barrier (BBB). Nuclear factor erythroid 2-related factor 2 (Nrf2) is a key transcription factor that plays a crucial role in cytoprotection against inflammation. The present study investigated the role of Nrf2 in upregulating of nuclear factor kappa B (NF-κB) activity, tumor necrosis factor-α (TNF-α), and MMP-9 after SCI. ⋯ We detected the wet/dry weight ratio of impaired spinal cord tissue, the activation of NF-κB, the mRNA and protein levels of TNF-α and MMP-9, and the enzyme activity of MMP-9. Nrf2 (-/-) mice were demonstrated to have more spinal cord edema, NF-κB activation, TNF-α production, and MMP-9 expression after SCI compared with the wild-type controls. The results suggest that Nrf2 may play an important role in limiting the upregulation of NF-κB activity, TNF-α, and MMP-9 in spinal cord after SCI.
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Mediators of inflammation · Jan 2010
Upregulation of TLR2/4 expression in mononuclear cells in postoperative systemic inflammatory response syndrome after liver transplantation.
To explore the relationship between Toll-like rpheral blood mononuclear cells (PBMC) and systemic inflammatory response syndrome (SIRS) in postoperative patients of liver transplantation (LT). ⋯ Upregulation of TLR2/4 expression on PBMC may contribute to the development of postoperative SIRS during perioperative period of LT.
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Mediators of inflammation · Jan 2010
Retracted PublicationFurther increase in the expression of activation markers on monocyte-derived dendritic cells in coronary artery disease patients with ectasia compared to patients with coronary artery disease alone.
Coronary artery ectasia (CAE) is defined as localized or diffuse dilation of the coronary arteries. There are scarce data about the role of dendritic cells in CAE development. In this study we investigated the activation markers on the surface of monocyte-derived dendritic cells (mDCs) in coronary artery disease (CAD) patients with or without CAE. ⋯ mDCs display an increased cell surface concentration of activation molecules in CAD patients with CAE compared to patients with CAD alone. DC activation may play an important role for CAE development in patients with CAD.
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Mediators of inflammation · Jan 2009
ReviewComplement inhibition as a proposed neuroprotective strategy following cardiac arrest.
Out-of-hospital cardiac arrest (OHCA) is a devastating disease process with neurological injury accounting for a disproportionate amount of the morbidity and mortality following return of spontaneous circulation. A dearth of effective treatment strategies exists for global cerebral ischemia-reperfusion (GCI/R) injury following successful resuscitation from OHCA. ⋯ Due to the profound impact of GCI/R injury following OHCA, and the relative lack of effective neuroprotective strategies for this pathologic process, complement inhibition provides an exciting opportunity to augment existing treatments to improve patient outcomes. To this end, this paper will explore the pathophysiology of complement-mediated GCI/R injury following OHCA.