Mediators of inflammation
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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.
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Mediators of inflammation · Jan 2009
Inflammatory profile of awake function-controlled craniotomy and craniotomy under general anesthesia.
Surgical stress triggers an inflammatory response and releases mediators into human plasma such as interleukins (ILs). Awake craniotomy and craniotomy performed under general anesthesia may be associated with different levels of stress. Our aim was to investigate whether those procedures cause different inflammatory responses. ⋯ This study suggests that awake function-controlled craniotomy does not cause a significantly different inflammatory response than craniotomy performed under general anesthesia. It is also likely that function-controlled craniotomy does not cause a greater emotional challenge than tumor resection under general anesthesia.
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Mediators of inflammation · Jan 2009
The effects of interleukin-1beta in tumor necrosis factor-alpha-induced acute pulmonary inflammation in mice.
We determined the role of interleukin-1beta (IL-1beta) signaling on tumor necrosis factor alpha-induced (TNF-alpha) lung neutrophil influx as well as neutrophil chemoattractant macrophage inflammatory protein (MIP-2) and KC and soluble TNF-alpha receptor (TNFR) levels utilizing wildtype (WT), TNF receptor double knockout (TNFR1/TNFR2 KO), and IL-1beta KO mice after oropharyngeal instillation with TNF-alpha. A significant increase in neutrophil accumulation in bronchoalveolar lavage fluid (BALF) and lung interstitium was detected in the WT mice six hours after TNF-alpha exposure. ⋯ TNF-alpha-instillation increased lavage and serum KC and soluble TNFR2 irrespective of IL-1beta expression. These results suggest IL-1beta contributes, in part, to TNF-alpha-mediated, chemokine release, and neutrophil recruitment to the lung, potentially associated with altered soluble TNFR1 release into the BALF.
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Mediators of inflammation · Jan 2009
Chemokine receptor and ligand upregulation in the diaphragm during endotoxemia and Pseudomonas lung infection.
Sepsis-induced diaphragmatic inflammation has been associated with respiratory failure, but the role of chemokines in this process has not been evaluated. Here we sought to study the local expression and molecular regulation of the chemokines, regulated upon activation normal T cell expressed and secreted (RANTES) and macrophage inflammatory protein (MIP)-1alpha, in the murine diaphragm during sepsis. Constitutive expression levels of RANTES and MIP-1alpha, as well as their receptors, CCR1 and CCR5, were significantly higher in diaphragm than limb muscle. ⋯ Inhibition of the NF-kB pathway using pharmacologic or dominant negative genetic approaches blocked the LPS-induced RANTES upregulation, while free radical scavengers had no effect. We conclude that sepsis leads to greatly increased expression of RANTES, MIP-1alpha and their cognate receptors in the diaphragm. Manipulation of the NF-kB pathway and other regulators of chemokine expression in the diaphragm could represent a novel method for mitigating the skeletal muscle inflammatory response associated with sepsis-induced diaphragmatic dysfunction.