scholarly journals The Effect of Sex-Mismatched Red Blood Cell Transfusion on Endothelial Cell Activation in Critically Ill Patients

2021 ◽  
pp. 1-8
Author(s):  
Abdulrahman Alshalani ◽  
Lisa van Manen ◽  
Margit Boshuizen ◽  
Robin van Bruggen ◽  
Jason P. Acker ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Blood Cell ◽  
Critically Ill ◽  
Red Blood Cell ◽  
Critically Ill Patients ◽  
Cell Activation ◽  
Endothelial Activation ◽  
Endothelial Cell Activation ◽  
Activation Markers ◽  
Matched Group

<b><i>Background:</i></b> Observational studies suggest that sex-mismatched transfusion is associated with increased mortality. Mechanisms driving mortality are not known but may include endothelial activation. The aim of this study is to investigate the effects of sex-mismatched red blood cell (RBC) transfusions on endothelial cell activation markers in critically ill patients. <b><i>Study Design and Methods:</i></b> In patients admitted to the intensive care unit who received a single RBC unit, blood samples were drawn before (T<sub>0</sub>), 1 h after (T<sub>1</sub>), and 24 h after transfusion (T<sub>24</sub>) for analysis of soluble syndecan-1, soluble intercellular adhesion molecule-1, soluble thrombomodulin (sTM), von Willebrand factor antigen, interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNFα). Changes in the levels of these factors were compared between sex-matched and sex-mismatched groups. <b><i>Results:</i></b> Of 69 included patients, 32 patients were in the sex-matched and 37 patients were in the sex-mismatched group. Compared to baseline, sex-matched transfusion was associated with significant reduction in sTM level (<i>p</i> value = 0.03). Between-group comparison showed that levels of syndecan-1 and sTM were significantly higher in the sex-mismatched group compared to the sex-matched group at T<sub>24</sub> (<i>p</i> value = 0.04 and 0.01, respectively). Also, TNFα and IL-6 levels showed a statistically marginal significant increase compared to baseline in the sex-mismatched group at T<sub>24</sub> (<i>p</i> value = 0.06 and 0.05, respectively), but not in the sex-matched group. <b><i>Discussion:</i></b> Transfusion of a single sex-mismatched RBC unit was associated with higher syndecan-1 and sTM levels compared to transfusion of sex-matched RBC unit. These findings may suggest that sex-mismatched RBC transfusion is associated with endothelial activation.

scholarly journals Effect of red blood cell transfusion on inflammation, endothelial cell activation and coagulation in the critically ill

Vox Sanguinis ◽  
2021 ◽  
Author(s):  
Lisa Manen ◽  
Maike E. Hezel ◽  
Margit Boshuizen ◽  
Marleen Straat ◽  
Angelique M. E. Man ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Blood Cell ◽  
Critically Ill ◽  
Red Blood Cell ◽  
Cell Activation ◽  
Red Blood Cell Transfusion ◽  
Endothelial Cell Activation

Abstract 66: The Role of the Viral Nef Protein as a Mediator of HIV-1--Induced Endothelial Dysfunction

2012 ◽  
Vol 111 (suppl_1) ◽  
Author(s):  
Ting Wang
Keyword(s):  
Cardiovascular Disease ◽  
T Cells ◽  
Endothelial Cells ◽  
Endothelial Cell ◽  
Endothelial Dysfunction ◽  
Binding Site ◽  
Cell Activation ◽  
Endothelial Activation ◽  
Endothelial Cell Activation ◽  
Hiv 1

With the prevalence of antiviral therapy in the developed world, many HIV-1-infected people die of diseases other than AIDS. One of the emerging major causes is cardiovascular disease, leading to the prediction that the majority of HIV-1 patients are expected to develop cardiovascular complications. Endothelial dysfunction is thought to be a key event in the development of cardiovascular diseases, particularly atherosclerosis. Assays testing the effect of HIV-1 on endothelial activation shows that direct contact with HIV-1 infected T cells enhance endothelial cell activation to a greater extent than HIV-1 alone, suggesting an intracellular HIV-1 protein is responsible for endothelial activation. The HIV-1 viral protein Nef, which is responsible for T cell activation and maintenance of high viral loads in vivo , has been shown to mediate its own transfer to bystander cells. We demonstrate here for the first time that Nef induces nanotube-like conduits connecting T cells and endothelial cells. We also show that Nef is transferred from T cells to endothelial cells via these nanotubes, and is necessary and sufficient for endothelial cell activation. Moreover, we show that SIV-infected macaques exhibit endothelial Nef expression in coronary arteries. Nef expression in endothelial cells causes endothelial apoptosis, ROS and MCP-1 production. Interestingly, a Nef SH3 binding site mutant abolishes Nef-induced apoptosis and ROS formation and reduces MCP-1 production in endothelial cells, suggesting that the Nef SH3 binding site is critical for Nef effects on endothelial cells. Nef induces apoptosis of endothelial cells through an NADPH oxidase- and ROS-dependent mechanism, while Nef-induced MCP-1 production is NF-kB dependent. Taken together, these data suggest that Nef can mediate its transfer from T cells to endothelial cells through nanotubes to enhance endothelial dysfunction.Thus, Nef is a promising new therapeutic target for reducing the risk for cardiovascular disease in the HIV-1 positive population.

scholarly journals Brucella abortus-Stimulated Platelets Activate Brain Microvascular Endothelial Cells Increasing Cell Transmigration through the Erk1/2 Pathway

Pathogens ◽  
2020 ◽  
Vol 9 (9) ◽  
pp. 708
Author(s):  
Ana María Rodríguez ◽  
Aldana Trotta ◽  
Agustina P. Melnyczajko ◽  
M. Cruz Miraglia ◽  
Kwang Sik Kim ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Brucella Abortus ◽  
Cell Activation ◽  
Transendothelial Migration ◽  
Endothelial Activation ◽  
Microvascular Endothelial Cell ◽  
Inflammatory Disorder ◽  
Endothelial Cell Activation ◽  
Microvascular Endothelial

Central nervous system invasion by bacteria of the genus Brucella results in an inflammatory disorder called neurobrucellosis. A common feature associated with this pathology is blood–brain barrier (BBB) activation. However, the underlying mechanisms involved with such BBB activation remain unknown. The aim of this work was to investigate the role of Brucella abortus-stimulated platelets on human brain microvascular endothelial cell (HBMEC) activation. Platelets enhanced HBMEC activation in response to B. abortus infection. Furthermore, supernatants from B. abortus-stimulated platelets also activated brain endothelial cells, inducing increased secretion of IL-6, IL-8, CCL-2 as well as ICAM-1 and CD40 upregulation on HBMEC compared with supernatants from unstimulated platelets. Outer membrane protein 19, a B. abortus lipoprotein, recapitulated B. abortus-mediated activation of HBMECs by platelets. In addition, supernatants from B. abortus-activated platelets promoted transendothelial migration of neutrophils and monocytes. Finally, using a pharmacological inhibitor, we demonstrated that the Erk1/2 pathway is involved in the endothelial activation induced by B. abortus-stimulated platelets and also in transendothelial migration of neutrophils. These results describe a mechanism whereby B. abortus-stimulated platelets induce endothelial cell activation, promoting neutrophils and monocytes to traverse the BBB probably contributing to the inflammatory pathology of neurobrucellosis.

Red blood cell transfusion is associated with decreased in-hospital muscle strength among critically ill patients requiring mechanical ventilation

2013 ◽  
Vol 28 (6) ◽  
pp. 1079-1085 ◽  
Author(s):  
Elizabeth C. Parsons ◽  
Erin K. Kross ◽  
Naeem A. Ali ◽  
Lisa K. Vandevusse ◽  
Ellen S. Caldwell ◽  
...  
Keyword(s):  
Mechanical Ventilation ◽  
Muscle Strength ◽  
Blood Cell ◽  
Critically Ill ◽  
Red Blood Cell ◽  
Critically Ill Patients ◽  
Red Blood Cell Transfusion

ANEMIA EVALUATION AND OUTCOME IN CRITICALLY ILL PATIENTS SUBMITTED TO A RED BLOOD CELL TRANSFUSION RESTRICTIVE POLICY.

2006 ◽  
Vol 34 ◽  
pp. A74
Author(s):  
Daniele M Torres ◽  
Rafael B Tomita ◽  
Maria Tereza M Ferrari ◽  
João M Silva ◽  
Luciano Sanches ◽  
...  
Keyword(s):  
Blood Cell ◽  
Critically Ill ◽  
Red Blood Cell ◽  
Critically Ill Patients ◽  
Red Blood Cell Transfusion ◽  
Restrictive Policy

scholarly journals Study protocol and pilot results of an observational cohort study evaluating effect of red blood cell transfusion on oxygenation and mitochondrial oxygen tension in critically ill patients with anaemia: the INsufficient Oxygenation in the Intensive Care Unit (INOX ICU-2) study

BMJ Open ◽  
2020 ◽  
Vol 10 (5) ◽  
pp. e036351 ◽  
Author(s):  
Meryem Baysan ◽  
Mendi S Arbous ◽  
Egbert G Mik ◽  
Nicole P Juffermans ◽  
Johanna G van der Bom
Keyword(s):  
Intensive Care ◽  
Blood Cell ◽  
Critically Ill ◽  
Red Blood Cell ◽  
Critically Ill Patients ◽  
Tissue Oxygenation ◽  
Protoporphyrin Ix ◽  
Oxygen Balance ◽  
Mixed Effect ◽  
Rbc Transfusion

IntroductionThe recently developed protoporphyrin IX-triple state lifetime technique measures mitochondrial oxygenation tension (mitoPO2) in vivo at the bedside. MitoPO2might be an early indicator of oxygen disbalance in cells of critically ill patients and therefore may support clinical decisions regarding red blood cell (RBC) transfusion. We aim to investigate the effect of RBC transfusion and the associated changes in haemoglobin concentration on mitoPO2 and other physiological measures of tissue oxygenation and oxygen balance in critically ill patients with anaemia. We present the protocol and pilot results for this study.Methods and analysisWe perform a prospective multicentre observational study in three mixed intensive care units in the Netherlands with critically ill patients with anaemia in whom an RBC transfusion is planned. The skin of the anterior chest wall of the patients is primed with a 5-aminolevulinic acid patch for 4 hours for induction of mitochondrial protoporphyrin-IX to enable measurements of mitoPO2, which is done with the COMET monitoring device. At multiple predefined moments, before and after RBC transfusion, we assess mitoPO2 and other physiological parameters of oxygen balance and tissue oxygenation. Descriptive statistics will be used to describe the data. A linear mixed-effect model will be used to study the association between RBC transfusion and mitoPO2 and other traditional parameters of oxygenation, oxygen delivery and oxygen balance. Missing data will be imputed using multiple imputation methods.Ethics and disseminationThe institutional ethics committee of each participating centre approved the study (reference P16.303), which will be conducted according to the 1964 Helsinki declaration and its later amendments. The results will be submitted for publication in peer-reviewed journals and presented at scientific conferences.Trial registration numberNCT03092297.

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