Soluble E-selectin is found in supernatants of activated endothelial cells and is elevated in the serum of patients with septic shock.

Newman, Walter; Beall, L D; Carson, Craig W.; Gg, Hunder; Graben, N; Randhawa, Zafar I.; Gopal, T V; Wiener-Kronish, Jeanine P.; Matthay, MA

doi:10.4049/jimmunol.150.2.644

Cited by 300 publications

(9 citation statements)

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“…The correlations between sE-cadherin and ESR and IL-6 suggest a potential relationship between sE-cadherin release and systemic inflammation in SLE. In accordance with these results, it has been shown that IL-1 causes shedding of E-cadherin from the cell surface of cultured human endothelial cells 32 . In a mouse model, intratracheal antigen or lipopolysaccharide challenge induced focal sE-cadherin release that was correlated with infiltrated neutrophil numbers 33 .…”

Section: Discussionsupporting

confidence: 78%

Soluble E-cadherin in Systemic Lupus Erythematosus

Jin

Almehed²,

Zhu³

et al. 2013

J Rheumatol

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Section: Discussionsupporting

confidence: 78%

Soluble E-cadherin in Systemic Lupus Erythematosus

Jin

Almehed²,

Zhu³

et al. 2013

J Rheumatol

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“…Soluble forms of E-selectin have been found in supernatants of cytokine-stimulated endothelial cells in culture [88,89]. Low serum levels are present in healthy subjects, and elevated levels were detected in patients with septic shock [89].…”

Section: Soluble Adhesion Moleculesmentioning

confidence: 99%

Endothelial Cells: Role in Infection and Inflammation

1998

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Infection and resulting sepsis continue to be important causes of morbidity and mortality in surgical patients. Although much has been learned about the pathogens and the leukocyte responses to these pathogens, we are only beginning to understand the role of the host in these pathologies. The endothelium is a dynamic participant in cellular and organ function rather than a static barrier as it was once believed. Emerging evidence implicates the endothelium as a central effector in the inflammatory response. Through the expression of surface proteins and secretion of soluble mediators, the endothelium controls vascular tone and permeability, regulates coagulation and thrombosis, and directs the passage of leukocytes into areas of inflammation. Derangements in these normal functions may contribute significantly to a maladaptive inflammatory response leading to systemic inflammation and multiple organ failure.

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“…Soluble E-selectin (sE) is present in the supernatants of cultured endothelial cells activated by interleukin-1␤, and the serum level of sE is elevated in patients with septic shock [8]. Thus, it is possible that serum levels of sE may reflect cytokine-induced endothelial cell activa-tion, which leads to disseminated intravascular coagulation (DIC) in the presence of sepsis.…”

Section: Introductionmentioning

confidence: 99%

Plasma levels of soluble E-selectin in patients with disseminated intravascular coagulation

et al. 1997

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The plasma level of soluble E-selectin (sE) reflects the activation of endothelial cells induced by cytokines such as tumor necrosis factor-and interleukin-1 in vitro. These cytokines are important in the development of coagulation abnormalities in patients with sepsis. We compared the plasma levels of sE in patients with infections suspected of having disseminated intravascular coagulation (DIC) (n = 33) and in patients with underlying disorders other than infections, including solid tumors (n = 28), obstetric disorders (n = 13), hematologic malignancies (n = 13), and liver disease (n = 9), to clarify the involvement of cytokines in the development of coagulation abnormalities in patients with sepsis. Plasma levels of sE in patients with infection were significantly higher than in patients with the other underlying disorders. The plasma level of sE was also significantly higher in patients with infection with DIC (114.6 ± 77.9 ng/ml, n = 21) than in patients with infection without DIC (54.5 ± 53.1 ng/ml, n = 12, P < 0.02). There was no significant difference in sE level between patients with the other underlying disorders with and without DIC. The plasma level of sE was significantly correlated with the serum level of FDP(E) in patients with infection. The plasma level of sE was significantly higher in patients with infection with organ failure compared to patients without organ failure. There was no significant difference between patients with the other underlying disorders with and without organ failure. Plasma levels of tumor necrosis factor-and interleukin-6 were detected in only 12.1% and 20.0% of patients with infections, respectively. These observations strongly suggest that plasma levels of sE reflect the activation of endothe-lial cells induced by cytokines, which may lead to DIC and organ failure in the presence of sepsis. Furthermore, determination of plasma level of sE may be useful for detecting the endothelial activation induced by cytokines in the pathologic conditions of sepsis, even when plasma levels of cytokines cannot be detected. Am.

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Soluble E-selectin is found in supernatants of activated endothelial cells and is elevated in the serum of patients with septic shock.

Cited by 300 publications

References 0 publications

Soluble E-cadherin in Systemic Lupus Erythematosus

Soluble E-cadherin in Systemic Lupus Erythematosus

Endothelial Cells: Role in Infection and Inflammation

Plasma levels of soluble E-selectin in patients with disseminated intravascular coagulation

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