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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Meta Analysis
Efficacy of supplemental hemoadsorption therapy on severe and critical patients with COVID-19: an evidence-based analysis.
Background: The COVID-19 pandemic has posed a disproportionately high threat to the global health system and social stability. COVID-19 damage can lead to hyperinflammation and tissue damage due to a "cytokine storm," which in turn contributes to an increase in the mortality rate. Extracorporeal hemoadsorption therapy (HAT) in patients with severe COVID-19 may improve organ function and stabilize hemodynamic status; however, the effects of supplemental HAT remain controversial. ⋯ Conclusion: Given the better mortality outcomes, HAT confers clinical benefits to patients with severe COVID-19, which correlated with cytokine removal by HAT. Cytokine adsorption may not provide clinical benefits for patients with severe COVID-19 requiring ECMO and should be used with caution. However, because of the very low quality of evidence, multicenter randomized trials with large sample sizes are required to verify these findings.
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The depletion of peripheral blood B cells is associated with immunosuppression and poor prognosis during sepsis, and selective depletion occurs when B cell subsets are specifically targeted. In this study, we examined the mechanisms underlying the selective depletion of B cell subsets in the immunosuppressive phase of septic shock patients. Thirty-two septic shock patients were recruited as a septic shock group and 10 healthy volunteers as a control group. ⋯ Activated caspase-1 levels in IM B cells were higher compared with activated caspase-3 in septic shock patients, whereas the levels of activated caspase-1 in AM B cells were lower compared with activated caspase-3. Moreover, in vitro experiments showed that Z-DEVD-FMK and VX-765 could alleviate the depletion of IM, AM, and RM B cells. The selective reduction of circulating B cell subsets in septic shock patients could be attributed to intrinsic and extrinsic apoptosis as well as pyroptosis.
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Background: Approximately 50% of patients with sepsis develop acute kidney injury (AKI), which is predictive of poor outcomes, with mortality rates of up to 70%. The endothelium is a major target for treatments aimed at preventing the complications of sepsis. We hypothesized that human umbilical cord-derived mesenchymal stem cells (hUC-MSCs) could attenuate tubular and endothelial injury in a porcine model of sepsis-induced AKI. ⋯ Expression of P-selectin, thrombomodulin, and vascular endothelial growth factor was significantly lower in the sepsis+MSC group than in the sepsis group, whereas that of Toll-like receptor 4 (TLR4) and nuclear factor-kappa B (NF-κB) was lower in the former. Conclusion: Treatment with hUC-MSCs seems to protect endothelial and tubular cells in sepsis-induced AKI, possibly via the TLR4/NF-κB signaling pathway. Therefore, it might be an effective treatment for sepsis-induced AKI.
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Background: Sepsis reduces neutrophil apoptosis. As the result, neutrophils may become aged, exacerbating inflammation and tissue injury. Extracellular cold-inducible RNA-binding protein (eCIRP) acts as a damage-associated molecular pattern to promote inflammation and tissue injury in sepsis. ⋯ We also found that aged neutrophils expressed significantly higher levels of SerpinB2 compared with non-aged neutrophils. Conclusions: eCIRP inhibits neutrophil apoptosis to increase aged phenotype by increasing SerpinB2 expression in sepsis. Thus, targeting eCIRP could be a new therapeutic strategy to ameliorate inflammation caused by neutrophil aging in sepsis.
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Nonantibody-mediated transfusion-related acute lung injury (TRALI) may account for up to 25% of TRALI cases. This indicates the need for further research to understand the pathophysiological mechanisms involved beyond antibody mediation fully. During this research, a TRALI rat model was developed using the trauma-blood loss-massive transfusion method. ⋯ In addition, HMGB1 and RIP3 promoted the inflammatory response by stimulating the toll-like receptor 44/nuclear factor kappa B and mitogen-activated protein kinase signaling pathways in the lung tissue of rats. Identifying efficient agents from inflammatory mediators such as alarmin can be an innovative scheme for diagnosing and preventing TRALI. These findings give HMGB1 and RIP3 a strong theoretical and experimental foundation for clinical use.