ArticleBritish journal of pharmacology2005
Differing mechanisms of leukocyte recruitment and sensitivity to conditioning by shear stress for endothelial cells treated with tumour necrosis factor-alpha or interleukin-1beta.
Article in British journal of pharmacology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 44 citations in OpenAlex.
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- Uncovering emergent phenotypes in endothelial cells by clustering of surrogates of cardiovascular risk factors.Scientific reports · 2022Article
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- ADAM10-Interacting Tetraspanins Tspan5 and Tspan17 Regulate VE-Cadherin Expression and Promote T Lymphocyte Transmigration.Journal of immunology (Baltimore, Md. : 1950) · 2017Article
- Shear stress upregulates IL-1β secretion by Chlamydia pneumoniae- infected monocytes.Biotechnology and bioengineering · 2015Article
- The role of the inflammasome in cardiovascular diseases.Journal of molecular medicine (Berlin, Germany) · 2014Review
- Flow-dependent Smad2 phosphorylation and TGIF nuclear localization in human aortic endothelial cells.American journal of physiology. Heart and circulatory physiology · 2011Article
- Delay of migrating leukocytes by the basement membrane deposited by endothelial cells in long-term culture.Experimental cell research · 2011Article
- Neutrophil adhesion on endothelial cells in a novel asymmetric stenosis model: effect of wall shear stress gradients.Annals of biomedical engineering · 2010Article
- Flow interactions with cells and tissues: cardiovascular flows and fluid-structure interactions. Sixth International Bio-Fluid Mechanics Symposium and Workshop, March 28-30, 2008, Pasadena, California.Annals of biomedical engineering · 2010Article
- Laminar shear stress regulates endothelial kinin B1 receptor expression and function: potential implication in atherogenesis.Arteriosclerosis, thrombosis, and vascular biology · 2009Article
- Spatial regulation of inflammation by human aortic endothelial cells in a linear gradient of shear stress.Microcirculation (New York, N.Y. : 1994) · 2008Article
- Morphological analysis of tumor cell/endothelial cell interactions under shear flow.Journal of biomechanics · 2007Article
- Chemokine- and adhesion-dependent survival of neutrophils after transmigration through cytokine-stimulated endothelium.Journal of leukocyte biology · 2006Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The cytokines tumour necrosis factor-alpha (TNFalpha) and interleukin-1beta (IL-1B) induce endothelial cells to recruit leukocytes. However, the exact adhesion and activation mechanisms induced by each cytokine, and their relative sensitivities to modulation by endothelial exposure to shear stress remain unclear. We cultured human umbilical vein endothelial cells (HUVEC) in glass capillaries at various shear stresses, with TNFalpha or IL-1B added for the last 4 h. Subsequently, human neutrophils were perfused over the HUVEC, and adhesion and migration were recorded. Both cytokines induced dose-dependent capture of neutrophils. However, while conditioning of HUVEC by increasing shear stress for 24 h diminished their response to TNFalpha, the response of HUVEC to IL-1B was similar at all shear stresses. The differing sensitivities were evident at levels of adhesive function and mRNA for adhesion molecules and chemokines. Analysis of nuclear factor kappaB (NF-kappaB)/Rel family of transcription factors showed that their expression and activation were modified by exposure to shear stress, but did not obviously explain differential responses to TNFalpha and IL-1B. Antibodies against selectins were effective against capture of neutrophils on TNFalpha-treated but not IL-1B-treated HUVEC. Stable adhesion was supported by beta2-integrins in each case. Activation of neutrophils occurred dominantly through CXC-chemokine receptor 2 (CXCR2) for TNFalpha-treated HUVEC, while blockade of CXCR1, CXCR2 and of platelet-activating factor receptors caused additive inhibition of migration on IL-1B-treated HUVEC. The mechanisms which underlie neutrophil recruitment, and their modulation by the haemodynamic environment, differ between cytokines. Interventions aimed against leukocyte recruitment may not operate equally in different inflammatory milieu.
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