Shock : molecular, cellular, and systemic pathobiological aspects and therapeutic approaches : the official journal the Shock Society, the European Shock Society, the Brazilian Shock Society, the International Federation of Shock Societies
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Blunt chest trauma is known to induce a pulmonary invasion of short-lived polymorphonuclear neutrophils and apoptosis of alveolar epithelial type 2 (AT2) cells. Apoptotic cells are removed by alveolar macrophages (AMΦ). We hypothesized that chest trauma alters the phagocytic response of AMΦ as well as the mediator release of AMΦ during phagocytosis. ⋯ These findings indicate that chest trauma augments the phagocytosis of apoptotic cells by AMΦ. Phagocytosis of opsonized beads enhances and ingestion of apoptotic cells downregulates the immunologic response following lung contusion. Our data emphasize the important role of phagocytosis during posttraumatic inflammation after lung contusion.
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A growing body of evidence indicates that anesthetic agents may play some roles in the cardiovascular and immune systems after injury. Myocardial anesthetic preconditioning is found to be involved in the anesthetic-induced cardioprotective effect. ⋯ Moreover, through anti-inflammatory effects and antioxidant properties, the anesthetic agents are believed to modulate immune response of individuals after injury. Thus, alteration or modulation of cardiovascular and immune function by the administration of anesthetic agents to the patients at the time of injury appears to be appropriate and important.
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Bacterial DNA (bDNA) contains hypomethylated "CpG" repeats that can be recognized by Toll-like receptor 9 (TLR-9) as a pathogen-associated molecular pattern. The ability of bDNA to initiate lung injury via TLR-9 has been inferred on the basis of studies using artificial CpG DNA. But the role of authentic bDNA in lung injury is still unknown. ⋯ Taken together, our results strongly support the conclusion that bDNA can initiate lung injury by stimulating PMN-EC adhesive interactions predisposing to endothelial permeability. Bacterial DNA stimulation of TLR-9 appears to promote enhanced gene expression of adhesion molecules in both cell types. This leads to PMN-EC cross-talk, which is required for injury to occur.
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Early compliance with the sepsis resuscitation bundle has been suggested to reduce mortality. However, few data are available about the impact of late compliance with the bundle on outcomes. The aim of this study was to assess whether the completion of the resuscitation bundle within the first 6 h after admission to the intensive care unit (ICU), but beyond the specific time limit of the various bundle interventions, is related to an improvement in survival. ⋯ Importantly, similar results were found after excluding all patients with severe sepsis (rapid responders) and those with refractory shock (nonresponders). The task with highest improvement was the achievement of central venous oxygen saturation 70% or greater in 39% of patients. Compliance with the resuscitation bundle even beyond the recommended time is associated with improvement in survival in patients with severe sepsis/septic shock.
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The objective was to examine the relationship of duration and magnitude of arterial hypotension to subsequent cellular immune suppression and cytokinemia in patients hospitalized with community-acquired pneumonia (CAP). We studied an observational cohort of 525 subjects hospitalized after presenting to the emergency department with radiographic and clinical signs of CAP. We compared the duration and magnitude of hypotension, using the cardiovascular Sequential Organ Failure Assessment (CV SOFA) subscore, to day 3 monocyte expression of human leukocyte antigen-DR (mHLA-DR), a previously validated marker of cellular immune suppression. ⋯ In patients admitted with CAP, arterial hypotension over the first 3 days is associated with markers of monocyte deactivation. The duration of exposure to hypotension may be more important than the magnitude, and monocyte deactivation correlates with IL-6 and IL-10 release. These results suggest that persistent hypotension might contribute to immunosuppression following septic shock.