Critical care : the official journal of the Critical Care Forum
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Editorial Comment
The role of natural killer cells in the pathogenesis of sepsis: the ongoing enigma.
The study by Souza-Fonseca-Guimaraes and colleagues in the previous issue of Critical Care shows several alterations in blood natural killer (NK) characteristics during human sepsis and systemic inflammatory response syndrome, including changes in NK cell numbers, Toll-like receptor (TLR) expression, and responsiveness to TLR agonists. This paper advances our knowledge of NK cell biology during sepsis and provides the background for future investigations.
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Editorial Comment
A rapidly progressing lymphocyte exhaustion after severe sepsis.
Septic syndromes induce immune alterations that have long been considered solely an overwhelming pro-inflammatory response. Increasing evidence now suggests that, after the first pro-inflammatory hours, sepsis is accompanied by the occurrence of a systemic immune failure. Here, novel perspectives regarding sepsis-induced lymphocyte alterations will be discussed in the context of a recently published study investigating overtime evolution of co-inhibitory lymphocyte receptor expressions in patients with severe sepsis.
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Editorial Comment
Please don't call me RI anymore; I may not be the one you think I am!
The previous issue of Critical Care reports new data on renal resistive index in critically ill patients. Although high renal resistive index may indeed be associated with acute kidney injury, the existence of several determinants of this index, of which renal resistance is only one among many, obscures the usefulness of this index in clinical practice.
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Editorial Comment
A lipid mediator controls neutrophil recruitment in acute lung injury - should we really be surprised?
New therapeutic approaches are sorely needed for acute lung injury. Neutrophil recruitment is a pathological hallmark of this syndrome, and is mainly regulated by CXC chemokine receptor 2 and its ligand CXC ligand 1. Rossaint and colleagues have described a new mechanism for regulation of this axis by 12/15-lipoxygenase products. This work opens the door for new therapeutic approaches and highlights the crucial interplay between lipid mediators and chemokines, a time-honored but often-ignored concept.
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Hemorrhagic shock induced O2 deficit triggers inflammation and multiple organ failure (MOF). Endogenous H2S has been proposed to be involved in MOF since plasma H2S concentration appears to increase in various types of shocks and to predict mortality. We tested the hypothesis that H2S increases during hemorrhagic shock associated with O2 deficit, and that enhancing H2S oxidation by hydroxocobalamin could reduce inflammation, O2 deficit or mortality. ⋯ In the presence of a large O2 deficit, H2S did not increase in the blood in a rat model of untreated hemorrhagic shock. Hydroxocobalamin, while effective against H2S in vitro, did not affect the hemodynamic profile or outcome in our model.