The Anti-Inflammatory Drug Nimesulide Inhibits Neutrophil Adherence to and Migration Across Monolayers of Cytokine-Activated Endothelial Cells

Respiration ◽  
1994 ◽  
Vol 61 (6) ◽  
pp. 336-341 ◽  
Author(s):  
Patrizia Dapino ◽  
Luciano Ottonello ◽  
Franco Dallegri
Keyword(s):  
Endothelial Cells ◽  
Inflammatory Drug ◽  
Neutrophil Adherence ◽  
Anti Inflammatory ◽  
And Migration

Extract of Housefly (Musca domestica) Maggot Anti-Inflammatory Parts could Regulate the Proliferation and Migration of TNF-α- Stimulated Human Umbilical Vein Endothelial Cells

2014 ◽  
Vol 884-885 ◽  
pp. 446-449
Author(s):  
Fu Jiang Chu ◽  
Hong Yan Ma ◽  
Xiao Bao Jin ◽  
Jia Yong Zhu
Keyword(s):  
Endothelial Cells ◽  
Treatment Group ◽  
Umbilical Vein ◽  
House Fly ◽  
Human Umbilical Vein ◽  
Tnf Α ◽  
Anti Inflammatory ◽  
And Migration ◽  
Umbilical Vein Endothelial Cells ◽  
Proliferation And Migration

House fly maggot, Musca domestica (Linnaeus) (Diptera: Muscidae) is one of the traditional Chinese medicine (TCM). In our earlier studies, the anti-inflammatory and anti-atherosclerotic functions of the housefly maggot have been found and also the anti-inflammatory effective parts have been acquired. In this study, the effect of housefly maggot anti-inflammatory parts on proliferation and migration of TNF-α-stimulated human umbilical vein endothelial cells (HUVEC) were investigated. And the results showed that the proliferation index and the migration rates of HUVEC which stimulated by TNF-α were decreased significantly in housefly maggot anti-inflammatory parts treatment group. And also the secretion of vascular endothelial growth factor (VEGF) was decreased too compared with only TNF-α treatment group. Based on the above, the housefly maggot anti-inflammatory parts could regulate the endothelial cell dysfunction through decreasing cell proliferation and migration and a reduction in VEGF expression might plays a key role in this process.

scholarly journals Neutrophil and monocyte adherence to and migration across monolayers of cytokine-activated endothelial cells: the contribution of CD18, ELAM-1, and VLA-4

Blood ◽  
1991 ◽  
Vol 78 (10) ◽  
pp. 2721-2726 ◽  
Author(s):  
BC Hakkert ◽  
TW Kuijpers ◽  
JF Leeuwenberg ◽  
JA van Mourik ◽  
D Roos
Keyword(s):  
Endothelial Cells ◽  
Leukocyte Adhesion ◽  
Interleukin 1 ◽  
Surface Proteins ◽  
Three Dimensional Model ◽  
Monocyte Migration ◽  
Combined Use ◽  
Neutrophil Adherence ◽  
And Migration ◽  
Monocyte Adherence

Pretreatment of endothelial cells with cytokines enhances the adherence of leukocytes, a process that is mediated by surface proteins expressed on both cell types. A three-dimensional model system for the simultaneous determination of leukocyte adherence and migration was used to study the contribution of CD11/CD18, endothelial leukocyte- adhesion molecule-1 (ELAM-1) and VLA-4 in neutrophil and monocyte adherence to and migration through cytokine-activated endothelial cells. Pretreatment of endothelial cells for 4 hours with recombinant interleukin-1 beta (rIL-1 beta) was found to enhance neutrophil adherence and migration to a much greater extent than monocyte adherence and migration. Neutrophil adherence was almost completely prevented by the combined use of monoclonal antibodies (MoAbs) against ELAM-1 and CD18. Although ELAM-1 has been designated an endothelial cell-specific cytokine-inducible receptor for neutrophils, we observed that ENA2, an anti-ELAM-1 MoAb, significantly reduced monocyte adherence about 30%. MoAbs against VLA-4, the ligand of the cytokine- inducible receptor VCAM-1, did not affect monocyte adherence. However, the combined use of the MoAbs against CD18, ELAM-1, and VLA-4 had a very strong and additive inhibitory effect on rIL-1 beta-induced monocyte adherence. The anti-CD18 MoAb reduced both rIL-1 beta-induced neutrophil and monocyte migration far below the level of the unstimulated controls, whereas neither the anti-ELAM-1 nor the anti-VLA- 4 MoAb significantly affected the process of migration. Our results indicate that neutrophils and monocytes initially adhere to cytokine- activated endothelial cells by CD18-independent and (to a lesser extent) by CD18-dependent mechanisms and subsequently change gears to a completely CD18-dependent migratory mechanism.

Assessment of Amphiphilic Poly-N-vinylpyrrolidone Nanoparticles’ Biocompatibility with Endothelial Cells in Vitro and Delivery of an Anti-Inflammatory Drug

2020 ◽  
Vol 17 (11) ◽  
pp. 4212-4225
Author(s):  
Aikaterini Berdiaki ◽  
Emmanouela Perisynaki ◽  
Antonios Stratidakis ◽  
Pavel P. Kulikov ◽  
Andrey N. Kuskov ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Inflammatory Drug ◽  
Anti Inflammatory

scholarly journals Neutrophil and monocyte adherence to and migration across monolayers of cytokine-activated endothelial cells: the contribution of CD18, ELAM-1, and VLA-4

Blood ◽  
1991 ◽  
Vol 78 (10) ◽  
pp. 2721-2726 ◽  
Author(s):  
BC Hakkert ◽  
TW Kuijpers ◽  
JF Leeuwenberg ◽  
JA van Mourik ◽  
D Roos
Keyword(s):  
Endothelial Cells ◽  
Leukocyte Adhesion ◽  
Interleukin 1 ◽  
Surface Proteins ◽  
Three Dimensional Model ◽  
Monocyte Migration ◽  
Combined Use ◽  
Neutrophil Adherence ◽  
And Migration ◽  
Monocyte Adherence

Abstract Pretreatment of endothelial cells with cytokines enhances the adherence of leukocytes, a process that is mediated by surface proteins expressed on both cell types. A three-dimensional model system for the simultaneous determination of leukocyte adherence and migration was used to study the contribution of CD11/CD18, endothelial leukocyte- adhesion molecule-1 (ELAM-1) and VLA-4 in neutrophil and monocyte adherence to and migration through cytokine-activated endothelial cells. Pretreatment of endothelial cells for 4 hours with recombinant interleukin-1 beta (rIL-1 beta) was found to enhance neutrophil adherence and migration to a much greater extent than monocyte adherence and migration. Neutrophil adherence was almost completely prevented by the combined use of monoclonal antibodies (MoAbs) against ELAM-1 and CD18. Although ELAM-1 has been designated an endothelial cell-specific cytokine-inducible receptor for neutrophils, we observed that ENA2, an anti-ELAM-1 MoAb, significantly reduced monocyte adherence about 30%. MoAbs against VLA-4, the ligand of the cytokine- inducible receptor VCAM-1, did not affect monocyte adherence. However, the combined use of the MoAbs against CD18, ELAM-1, and VLA-4 had a very strong and additive inhibitory effect on rIL-1 beta-induced monocyte adherence. The anti-CD18 MoAb reduced both rIL-1 beta-induced neutrophil and monocyte migration far below the level of the unstimulated controls, whereas neither the anti-ELAM-1 nor the anti-VLA- 4 MoAb significantly affected the process of migration. Our results indicate that neutrophils and monocytes initially adhere to cytokine- activated endothelial cells by CD18-independent and (to a lesser extent) by CD18-dependent mechanisms and subsequently change gears to a completely CD18-dependent migratory mechanism.

Anti-inflammatory effects of pelargonidin on TGFBIp-induced responses

2017 ◽  
Vol 95 (4) ◽  
pp. 372-381 ◽  
Author(s):  
Seongdo Jeong ◽  
Sae-Kwang Ku ◽  
Jong-Sup Bae
Keyword(s):  
Endothelial Cells ◽  
Cell Adhesion ◽  
Adhesion Molecules ◽  
Cell Adhesion Molecules ◽  
Matrix Protein ◽  
Biological Activities ◽  
Extracellular Matrix Protein ◽  
Experimental Sepsis ◽  
Anti Inflammatory ◽  
And Migration

Transforming growth factor β induced protein (TGFBIp) is an extracellular matrix protein expressed in several cell types in response to TGF-β. TGFBIp is released by human umbilical vein endothelial cells (HUVECs) and functions as a mediator of experimental sepsis. Pelargonidin (PEL) is a well-known red pigment found in plants, and has been reported as having important biological activities that are potentially beneficial for human health. This study was undertaken to investigate whether PEL can modulate TGFBIp-mediated inflammatory responses in HUVECs and in mice. The anti-inflammatory activities of PEL were determined by measuring permeability, leukocyte adhesion and migration, and activation of proinflammatory proteins in TGFBIp-activated HUVECs and mice. In addition, the beneficial effects of PEL on survival rate in a mouse sepsis model were tested. We found that PEL inhibited TGFBIp-induced barrier disruption, expression of cell adhesion molecules and adhesion/transendothelial migration of neutrophils to human endothelial cells. PEL also suppressed TGFBIp-induced hyperpermeability and leukocyte migration in vivo. These results suggest that PEL possesses anti-inflammatory properties that result in inhibition of hyperpermeability, expression of cell adhesion molecules, and adhesion and migration of leukocytes, thereby endorsing its usefulness as a therapy for vascular inflammatory diseases.

Anti-inflammatory effects of dabrafenib in vitro and in vivo

2017 ◽  
Vol 95 (6) ◽  
pp. 697-707 ◽  
Author(s):  
In-Chul Lee ◽  
Jongdoo Kim ◽  
Jong-Sup Bae
Keyword(s):  
Endothelial Cells ◽  
Inflammatory Responses ◽  
Drug Repositioning ◽  
Umbilical Vein ◽  
Bioactive Compound ◽  
Compound Libraries ◽  
Anti Inflammatory ◽  
And Migration

The screening of bioactive compound libraries can be an effective approach for repositioning FDA-approved drugs or discovering new treatments for human diseases (drug repositioning). Drug repositioning refers to the development of existing drugs for new indications. Dabrafenib (DAB) is a B-Raf inhibitor and initially used for the treatment of metastatic melanoma therapy. Here, we tested the possible use of DAB in the treatment of lipopolysaccharide (LPS)-mediated vascular inflammatory responses. The anti-inflammatory activities of DAB were determined by measuring permeability, neutrophils adhesion and migration, and activation of pro-inflammatory proteins in LPS-activated human umbilical vein endothelial cells (HUVECs) and mice. We found that DAB inhibited LPS-induced barrier disruption, expression of cell adhesion molecules (CAMs), and adhesion and transendothelial migration of neutrophils to human endothelial cells. DAB also suppressed LPS-induced hyperpermeability and leukocytes migration in vivo. Furthermore, DAB suppressed the production of tumor necrosis factor-α (TNF-α) or interleukin (IL)-6 and the activation of nuclear factor-κB (NF-κB) or extracellular regulated kinases (ERK) 1/2 by LPS. Moreover, treatment with DAB resulted in reduced LPS-induced lethal endotoxemia. These results suggest that DAB possesses anti-inflammatory functions by inhibiting hyperpermeability, expression of CAMs, and adhesion and migration of leukocytes, thereby endorsing its usefulness as a therapy for vascular inflammatory diseases.

scholarly journals Neutrophil migration across monolayers of cytokine-prestimulated endothelial cells: a role for platelet-activating factor and IL-8.

1992 ◽  
Vol 117 (3) ◽  
pp. 565-572 ◽  
Author(s):  
T W Kuijpers ◽  
B C Hakkert ◽  
M H Hart ◽  
D Roos
Keyword(s):  
Endothelial Cells ◽  
Neutrophil Migration ◽  
Platelet Activating Factor ◽  
Human Neutrophils ◽  
Neutrophil Adherence ◽  
Paf Receptor ◽  
And Migration ◽  
Web 2086 ◽  
Paf Receptor Antagonist

In a previous study we observed that neutrophils respond with a rapid rise in [Ca2+]i during adherence to cytokine-activated endothelial cells (EC), caused by EC membrane-associated platelet-activating factor (PAF). In the present study, we investigated whether this form of PAF was important in neutrophil adherence and migration across monolayers of rIL-1 beta- or rTNF alpha-prestimulated EC. PAF receptor antagonists prevented neutrophil migration across cytokine-pretreated EC by approximately 60% (P less than 0.005) without interfering with the process of adherence. The antagonists WEB 2086 and L-652,731 had no effect on neutrophil migration across resting EC induced by formylmethionyl-leucyl-phenylalanine (FMLP). A murine anti-IL-8 antiserum was found to also partially inhibit the neutrophil transmigration across cytokine-activated EC. When the anti-IL-8 antiserum was used in combination with a PAF receptor antagonist, neutrophil migration across cytokine-pretreated monolayers of EC was completely prevented. During transmigration, LAM-1 and CD44 on the neutrophils were down-modulated; both WEB 2086 and anti-IL-8 antiserum partially prevented this down-modulation caused by cytokine-prestimulated EC. Our results indicate that human neutrophils are activated and guided by EC-associated PAF and EC-derived IL-8 during the in vitro diapedesis in between cytokine-stimulated EC.

Sign in / Sign up

Export Citation Format

Share Document