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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Polymorphonuclear granulocytes (PMNs) have been attributed a primarily deleterious role in the pathogenesis of acute lung injury (ALI). However, evidence exists that PMNs might also act beneficially in certain types of ALI. In this regard, we investigated the role of activated neutrophils in the pathophysiology of lung contusion-induced ALI. ⋯ In the presence of PMNs, BAL protein was further increased at 30 h when compared with the 3-h time point, which was not the case in the absence of PMNs. Taken together, in response to lung trauma, activated neutrophils control inflammation including mediator release from distant immune cells but simultaneously mediate pulmonary tissue damage. Thus, keeping in mind potential inflammatory adverse effects, modulation of neutrophil activation or trafficking might be a reasonable therapeutic approach in chest trauma-induced lung injury.
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The treatment of acute lung injury and septic complications after blunt chest trauma remains a challenge. Inhaled hydrogen sulfide (H₂S) may cause a hibernation-like metabolic state, which refers to an attenuated systemic inflammatory response. Therefore, we tested the hypothesis that inhaled H₂S-induced suspended animation may attenuate the inflammation after pulmonary contusion. ⋯ Furthermore, H₂S inhalation partially attenuated the mediator release in BAL and culture supernatants of Kupffer cells as well as splenic cells; it altered plasma cytokine concentrations but did not affect the trauma-induced changes in mononuclear cell culture supernatants. These findings indicate that inhaled H₂S induced a reduced metabolic expenditure and partially attenuated inflammation after trauma. Nevertheless, in contrast to hypoxic- or pathogen-induced lung injury, H₂S treatment appears to have no protective effect after blunt chest trauma.
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Hypothermia is considered an independent predictor of death after trauma. The aim of this study was to assess these premises based on data from the TraumaRegistry DGU® (TR-DGU) using its outcome predication tool, the Revised Injury Severity Classification (RISC) score, in comparison with three previously published regression models by Shafi, Martin, and Wang. We hypothesized that body temperature on admission would improve accuracy of the RISC score. ⋯ Comparison of the above models revealed hypothermia as an independent risk factor (Martin: OR, 1.43 [95% CI, 2.21-1.42*]; and Wang: OR, 1.77 [95% CI, 2.21-1.42*]) only, although it would drop out from the model (RISC: OR, 1.12 [95% CI, 1.41-0.89; P = 0.33] and Shafi: OR, 1,.21 [95% CI, 1.60-0.92; P = 0.17]) as long as parameters to indicate hemorrhage and/or coagulopathy were included in sufficient number, a finding confirmed by a subsequent sensitivity analysis. We conclude that hypothermia is a result of injury severity and therefore unlikely to be an independent predictor of mortality. Our data suggest that hypothermia belongs closely to the hemorrhage/coagulopathy group of predictors.
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Immunosuppressive signaling via the adenosine A2A receptor (A2AR) is an important pathway to control inflammation. In immune cells, expression levels of A2ARs influence responsiveness to inflammatory stimuli. However, mechanisms driving expressional changes of A2ARs are still largely elusive. ⋯ In PMNs, the increase in A2AR mRNA expression upon stimulation was inversely correlated with the expression levels of miRNA-214, miRNA-15, and miRNA-16 (R = -0.87, P < 0.0001); no correlation was found in human T cells. These results indicate that individual miRNA profiles gain important influence on A2AR expression regulation in PMNs upon stimulation. Determination of miRNA expression levels may help to identify patients with an increased risk for severe inflammation.
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Septic shock is the most common cause of death in intensive care units. During the last two decades, new strategies have focused on the diagnosis and on the immunological changes in critically ill patients. There have been conflicting reports whether monocyte human leukocyte antigen (HLA) DR expression poses a useful parameter to characterize clinical outcome of these patients. ⋯ As expected, HLA-DR expression was significantly higher in the group of survivors (n = 279) than in the group of nonsurvivors (n = 134; mABs/cell: 23,038 [SD, 11,150] vs. 18,070 [SD, 8,906]; P < 0.001). When minimal HLA-DR values per patient were compared, no cutoff values could be identified between the groups of survivors and nonsurvivors (mABs/cell: 19,611 [SD, 11,129] vs. 14,944 [SD, 8,013]; P < 0.001). In conclusion, in this sizable cohort we could again show that HLA-DR expression is decreased in critically ill patients but it is not suitable as a prognostic or predictive parameter for clinical outcome.