Circulating endothelial progenitor cells may predict outcomes in adult patients with severe sepsis in the emergency department

Kung, Chia-Te; Su, Chih-Min; Chen, Chao Tung; Cheng, Hsien-Hung; Chang, Meng-Wei; Hung, Chung-Chan; Hung, Shin-Chiang; Chang, Wen-Neng; Tsai, Nai‐Wen; Wang, Hung-Chen; Su, Yu‐Jih; Huang, Chung‐Cheng; Lin, Wei-Che; Cheng, Ben-Chung; Chang, Ya‐Ting; Lu, Cheng-Hsien

doi:10.1016/j.cca.2016.01.015

Cited by 17 publications

(12 citation statements)

References 31 publications

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“…We could in our previous studies already demonstrate that septic patients exhibit increased levels of circulating endothelial progenitor cells themselves, using FACS analysis[ 8 ]. Other groups have confirmed these results in human studies using the flow cytometry to analyze and count endothelial progenitors [ 30 – 32 ]; besides human studies, Luo et al showed an increase of circulating vascular stem cells in the early phase of endotoxemia induced sepsis in pigs with a peak after 72 hours [ 33 ]. However, studies based on the isolation of vascular progenitor cells by colony forming assays instead of flow cytometry did not show a significant increase in progenitor cell mobilization in sepsis [ 34 , 35 ].…”

Section: Discussionmentioning

confidence: 86%

“…Several human and animal studies have demonstrated higher numbers of vascular stem cells in survivors of sepsis [ 30 , 31 , 33 ]. Contrary to that, the research group of Kung et al recently saw a negative association between sepsis survival and endothelial progenitor cell numbers [ 32 ]. In the light of this controversy, our current data revealed slightly higher CD34 + /CD133 + -stem cell counts in sepsis-surviving patients, however, this difference was not significant.…”

Section: Discussionmentioning

confidence: 99%

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VCAM-1 expression is upregulated by CD34+/CD133+-stem cells derived from septic patients

et al. 2018

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CD34+/CD133+- cells are a bone marrow derived stem cell population, which presumably contain vascular progenitor cells and are associated with improved vascular repair. In this study, we investigated whether the adhesion molecules ICAM-1 (intercellular adhesion molecule-1), VCAM-1 (vascular adhesion molecule-1), E-selectin und L-selectin, which are involved in homing of vascular stem cells, are upregulated by CD34+/CD133+-stem cells from septic patients and would be associated with improved clinical outcome. Peripheral blood mononuclear cells from intensive care unit (ICU) patients with (n = 30) and without sepsis (n = 10), and healthy volunteers (n = 15) were isolated using Ficoll density gradient centrifugation. The expression of VCAM-1, ICAM-1, E-selectin and L-selectin was detected on CD34+/CD133+-stem cells by flow cytometry. The severity of disease was assessed by the Simplified Acute Physiology Score (SAPS) II. Serum concentrations of vascular endothelial growth factor (VEGF) and angiopoietin (Ang)-2 were determined by Enzyme-linked immunosorbent assay. The expression of VCAM-1, ICAM-1, E-selectin and L-selectin by CD34+/CD133+-stem cells was significantly upregulated in septic patients, and correlated with sepsis severity. Furthermore, high expression of VCAM-1 by CD34+/CD133+-stem cells revealed a positive association with mortalitiy (p<0.05). Furthermore, significantly higher serum concentrations of VEGF and Ang-2 were found in septic patients, however none showed a strong association with survival. Our data suggest, that VCAM-1 upregulation on CD34+/CD133+-stem cells could play a crucial role in their homing in the course of sepsis. An increase in sepsis severity resulted in both and increase in CD34+/CD133+-stem cells and VCAM-1-expression by those cells, which might reflect an increase in need for vascular repair.

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Section: Discussionmentioning

confidence: 86%

Section: Discussionmentioning

confidence: 99%

VCAM-1 expression is upregulated by CD34+/CD133+-stem cells derived from septic patients

et al. 2018

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“…Several research groups including our own have demonstrated, that septic patients and animals exhibit increased levels of circulating EPC and that there is a positive correlation with survival. EPC numbers have been analysed and calculated in these studies using flowcytometry [ 7 – 10 , 38 ]. However, in conflict with these findings, studies based on colony forming assays for EPC number analysis indicate, that EPC mobilization during sepsis is not enhanced [ 39 , 40 ].…”

Section: Discussionmentioning

confidence: 99%

CXCR-4 expression by circulating endothelial progenitor cells and SDF-1 serum levels are elevated in septic patients

et al. 2018

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BackgroundEndothelial progenitor cell (EPC) numbers are increased in septic patients and correlate with survival. In this study, we investigated, whether surface expression of chemokine receptors and other receptors important for EPC homing is upregulated by EPC from septic patients and if this is associated with clinical outcome.MethodsPeripheral blood mononuclear cells from septic patients (n = 30), ICU control patients (n = 11) and healthy volunteers (n = 15) were isolated by Ficoll density gradient centrifugation. FACS-analysis was used to measure the expression of the CXC motif chemokine receptors (CXCR)-2 and − 4, the receptor for advanced glycation endproducts (RAGE) and the stem cell factor receptor c-Kit. Disease severity was assessed via the Simplified Acute Physiology Score (SAPS) II. The serum concentrations of vascular endothelial growth factor (VEGF), stromal cell-derived factor (SDF)-1α and angiopoietin (Ang)-2 were determined with Enzyme linked Immunosorbent Assays.ResultsEPC from septic patients expressed significantly more CXCR-4, c-Kit and RAGE compared to controls and were associated with survival-probability. Significantly higher serum concentrations of VEGF, SDF-1α and Ang-2 were found in septic patients. SDF-1α showed a significant association with survival.ConclusionsOur data suggest that SDF-1α and CXCR-4 signaling could play a crucial role in EPC homing in the course of sepsis.Electronic supplementary materialThe online version of this article (10.1186/s12950-018-0186-7) contains supplementary material, which is available to authorized users.

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“…Reduced EPC counts have been found in pathological conditions that concur with endothelial dysfunction, including patients with depression with and without acute coronary syndromes. 15 , 17 , 34 , 35 , 36 In addition, presence of increased CECs is associated with endothelial damage. 14 Our study confirms that this pattern is also present in our patients.…”

Section: Discussionmentioning

confidence: 99%

Endothelial damage in major depression patients is modulated by SSRI treatment, as demonstrated by circulating biomarkers and an in vitro cell model

et al. 2016

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There is a link between depression, cardiovascular events and inflammation. We have explored this connection through endothelial dysfunction, using in vivo and in vitro approaches. We evaluated circulating biomarkers of endothelial dysfunction in patients with major depression at their diagnosis (MD-0) and during antidepressant treatment with the selective serotonin reuptake inhibitor escitalopram, for 8 and 24 weeks (MD-8 and MD-24). Results were always compared with matched healthy controls (CON). We measured in vivo circulating endothelial cells (CECs) and endothelial progenitor cells (EPCs) in blood samples, and assessed plasma levels of soluble von Willebrand factor (VWF) and vascular cell adhesion molecule-1 (VCAM-1). CEC counts, soluble VWF and VCAM-1 were statistically elevated in MD-0 (P<0.01 versus CON) and gradually decreased during treatment. Conversely, EPC levels were lower in MD-0, tending to increase throughout treatment. In vitro studies were performed in human endothelial cells cultured in the presence of sera from each study group. Elevated expression of the inflammation marker intercellular adhesion molecule-1 and oxidative stress, with lower presence of endothelial nitric oxide synthase and higher reactive oxygen species production, were found in cells exposed to MD-0 sera (P<0.05 versus CON). These results were normalized in cells exposed to MD-24 sera. Thrombogenicity of extracellular matrices generated by these cells, measured as expression of VWF, tissue factor and platelet reactivity, showed non-significant differences. We provide a model of cultured endothelial cells reproducing endothelial dysfunction in naive patients with major depression, demonstrating endothelial damage and inflammation at diagnosis, and recovering with selective serotonin reuptake inhibitor treatment for 24 weeks.

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Circulating endothelial progenitor cells may predict outcomes in adult patients with severe sepsis in the emergency department

Cited by 17 publications

References 31 publications

VCAM-1 expression is upregulated by CD34+/CD133+-stem cells derived from septic patients

VCAM-1 expression is upregulated by CD34+/CD133+-stem cells derived from septic patients

CXCR-4 expression by circulating endothelial progenitor cells and SDF-1 serum levels are elevated in septic patients

Endothelial damage in major depression patients is modulated by SSRI treatment, as demonstrated by circulating biomarkers and an in vitro cell model

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