Upregulation of intercellular adhesion molecule-1 (ICAM-1) expression in primary cultures of human brain microvessel endothelial cells by cytokines and lipopolysaccharide

Wong, Donald; Dorovini-Zis, Katerina

doi:10.1016/0165-5728(92)90170-p

Cited by 274 publications

(97 citation statements)

References 24 publications

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“…4,5 Consistent with this mechanistic model, analysis of various neuroinflammatory molecules (NMs) shows an initial marked enhancement, persistence, and subsequent depletion with time in animal models of brain abscess. [5][6][7][8] Some of these findings have been reproduced in human brain cells, for example, TNF-␣ and IL1-␤ induce ICAM-1 expression in human brain endothelial cells. [6][7][8] Diffusion tensor imaging (DTI) is a relatively new MR imaging technique that has been shown to provide tissue microstructural information.…”

mentioning

confidence: 85%

“…[5][6][7][8] Some of these findings have been reproduced in human brain cells, for example, TNF-␣ and IL1-␤ induce ICAM-1 expression in human brain endothelial cells. [6][7][8] Diffusion tensor imaging (DTI) is a relatively new MR imaging technique that has been shown to provide tissue microstructural information. 9 The commonly used DTI-derived metrics are fractional anisotropy (FA) and mean diffusivity (MD).…”

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confidence: 85%

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In Vivo Demonstration of Neuroinflammatory Molecule Expression in Brain Abscess with Diffusion Tensor Imaging

Gupta¹,

Nath²,

Prasad³

et al. 2008

American Journal of Neuroradiology

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confidence: 85%

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confidence: 85%

In Vivo Demonstration of Neuroinflammatory Molecule Expression in Brain Abscess with Diffusion Tensor Imaging

Gupta¹,

Nath²,

Prasad³

et al. 2008

American Journal of Neuroradiology

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“…ICAM-1 plays important functions in leukocyte transmigration through vessels, cell to cell adhesion impacting immune responsiveness during infections and disease pathogenesis. The level of membrane expression of ICAM on endothelia and MSCs is up-regulated by pro-inflammatory cytokines (IL-1, IL-6, TNFα) and IFNγ from activated T cells [204,206,207] and does not depend on intercellular adhesion. Generally, MSCs are renowned for their immune-suppressive function which is crucially dependent on membrane expression of ICAM-1, as demonstrated in a mouse experimental model.…”

Section: Intercellular Adhesion Moleculementioning

confidence: 99%

Secretion of immunoregulatory cytokines by mesenchymal stem cells

Kyurkchiev

Bochev

Ivanova‐Todorova

et al. 2014

WJSC

520

392

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According to the minimal criteria of the International Society of Cellular Therapy, mesenchymal stem cells (MSCs) are a population of undifferentiated cells defined by their ability to adhere to plastic surfaces when cultured under standard conditions, express a certain panel of phenotypic markers and can differentiate into osteogenic, chondrogenic and adipogenic lineages when cultured in specific inducing media. In parallel with their major role as undifferentiated cell reserves, MSCs have immunomodulatory functions which are exerted by direct cell-to-cell contacts, secretion of cytokines and/or by a combination of both mechanisms. There are no convincing data about a principal difference in the profile of cytokines secreted by MSCs isolated from different tissue sources, although some papers report some quantitative but not qualitative differences in cytokine secretion. The present review focuses on the basic cytokines secreted by MSCs as described in the literature by which the MSCs exert immunodulatory effects. It should be pointed out that MSCs themselves are objects of cytokine regulation. Hypothetical mechanisms by which the MSCs exert their immunoregulatory effects are also discussed in this review. These mechanisms may either influence the target immune cells directly or indirectly by affecting the activities of predominantly dendritic cells. Chemokines are also discussed as participants in this process by recruiting cells of the immune systems and thus making them targets of immunosuppression. This review aims to present and discuss the published data and the personal experience of the authors regarding cytokines secreted by MSCs and their effects on the cells of the immune system. © 2014 Baishideng Publishing Group Inc. All rights reserved.Key words: Mesenchymal stem cells; Immunomodulation; Cytokines; Chemokines; Dendritic cells Core tip: Autoimmune diseases affect approximately 5% of the human population, leading to serious disability and effective methods to treat these diseases are still not perfect. Mesenchymal stem cells (MSCs) are assumed to be promising agents, both for regenerative medicine and cell therapy for autoimmune disorders. Under the influence of some factors, mesenchymal stem cells secrete cytokines which induce suppression of the immune response. Studies on the secreted cytokines and the precise mechanisms involved in these suppressive mechanisms would create possibilities for efficient application of MSCs as a therapeutic means for treatment of autoimmune diseases.Kyurkchiev D, Bochev I, Ivanova-Todorova E, Mourdjeva M, REVIEWSubmit a

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“…Levels of sVCAM-1 were still elevated at 4 weeks post-MI. Interestingly, the results of recent in vitro studies showed that E-selectin was upregulated only transiently during the first hours after cytokine or thrombin stimulation, whereas immunoglobulin-type adhesion molecules were persistently expressed at cellular surfaces for at least 72 h. 18,19 Several of these adhesion molecules have been examined in patients with AMI. 20,21 Shyu et al reported that the serum levels of ICAM-1 were higher in patients with AMI than in control subjects, but there was no difference in the levels of patients with stable angina, 20 which was comparable to our results.…”

Section: Time-course and Role Of Adhesion Moleculesmentioning

confidence: 99%

Role of Cytokines and Adhesion Molecules in Ischemia and Reperfusion in Patients With Acute Myocardial Infarction

et al. 1999

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he most important cause of acute myocardial infarction (AMI) is plaque rupture in the coronary arteries with subsequent thrombosis. The risk of plaque rupture appears to be related to the composition of the atherosclerotic plaque. The same population of bloodderived monocytes/macrophages that transforms the atherosclerotic lesions into foam cells interacts with T lymphocytes and smooth muscle cells via growth factors and cytokines. 1 At the site of plaque rupture or erosion, inflammation processes play a role in destabilizing the fibrous cap tissue, thus enhancing the risk of coronary thrombosis. 2 However, the precise mechanisms causing plaque rupture are not fully understood. A large body of evidence points to the involvement of an inflammatory response in the pathophysiology of myocardial ischemia-reperfusion injury. 3 Leukocyte accumulation in the myocardium may amplify tissue damage by activating cardiomyocytes and by releasing deleterious substances such as inflammatory cytokines, 4,5 thromboxane A2, 6 oxygen-free radicals 7 and platelet activating factor (PAF). 8 Leukocytes and endothelium express adhesion molecules when stimulated, for example by cytokines, and their expression is considered to play a pivotal role in the localization and development of an inflammatory reaction. E-selectin as a selectin-type adhesion molecule, vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1) are immunoglobulin-type adhesion molecules, which are located on the surface of activated endothelial cells and bind leukocytes. Previous animal studies have clearly demonstrated that PAF antagonists, 9 and inhibition of ICAM-1 10,11 and selectin-type adhesion molecules 12 using monoclonal antibodies, significantly reduce the degree of myocardial injury that results from coronary artery occlusion and reperfusion. The aim of this study was to characterize these soluble adhesion molecules, PAF and interleukin-6 as inflammatory cytokines in patients with AMI in order to examine the possible role of these factors in the pathophysiology of AMI. Methods Study PatientsThe blood PAF levels were measured in 8 consecutive patients with AMI who were admitted within 12 h of the onset of symptoms and in 98 normal volunteers (Control). The study patients with AMI consisted of 6 men and 2 women, ranging in age from 47 to 79 years, with a mean age of 62.2±10.4 (mean ± SD) years (Study 1). We also measured the plasma levels of interleukin-6, soluble Eselectin (sE-selectin), soluble ICAM-1 (sICAM-1) and soluble VCAM-1 (sVCAM-1) in 30 patients with AMI who were admitted within 12 h of the onset of symptoms and in 15 patients with stable effort angina (SEA). The patients with AMI consisted of 26 men and 4 women, ranging in age from 30 to 80 years, with a mean age of Jpn Circ J 1999; 63: 362 -366 (Received August 31, 1998; revised manuscript received January 29, 1999; accepted February 5, 1999 Although acute myocardial infarction (AMI) may involve both plaque rupture and ischemia-reperfusion injury, the pathogenes...

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Upregulation of intercellular adhesion molecule-1 (ICAM-1) expression in primary cultures of human brain microvessel endothelial cells by cytokines and lipopolysaccharide

Cited by 274 publications

References 24 publications

In Vivo Demonstration of Neuroinflammatory Molecule Expression in Brain Abscess with Diffusion Tensor Imaging

In Vivo Demonstration of Neuroinflammatory Molecule Expression in Brain Abscess with Diffusion Tensor Imaging

Secretion of immunoregulatory cytokines by mesenchymal stem cells

Role of Cytokines and Adhesion Molecules in Ischemia and Reperfusion in Patients With Acute Myocardial Infarction

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