scholarly journals Ulmus davidiana ethanol extract inhibits monocyte adhesion to tumor necrosis factor-alpha-stimulated endothelial cells

2016 ◽  
Vol 5 (2) ◽  
pp. 131-139 ◽  
Author(s):  
Ki Mo Lee ◽  
Hee Kyoung Joo ◽  
Yu Ran Lee ◽  
Myoung Soo Park ◽  
Gun Kang ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Ethanol Extract ◽  
Monocyte Adhesion ◽  
Necrosis Factor Alpha ◽  
Factor Alpha ◽  
Ulmus Davidiana ◽  
Necrosis Factor

scholarly journals Regulation of thrombomodulin by tumor necrosis factor-alpha: comparison of transcriptional and posttranscriptional mechanisms

Blood ◽  
1991 ◽  
Vol 77 (3) ◽  
pp. 542-550 ◽  
Author(s):  
SR Lentz ◽  
M Tsiang ◽  
JE Sadler
Keyword(s):  
Endothelial Cells ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Posttranscriptional Regulation ◽  
Tumor Necrosis ◽  
Vascular Endothelial Cells ◽  
Necrosis Factor Alpha ◽  
Subsequent Decrease ◽  
Factor Alpha ◽  
Necrosis Factor

Abstract The procoagulant properties of cultured vascular endothelial cells are enhanced in response to inflammatory cytokines such as tumor necrosis factor-alpha (TNF). A major component of this response is a reduction in expression of thrombomodulin, a cell surface cofactor for the activation of protein C. Regulation of thrombomodulin expression by TNF has been reported to occur through multiple mechanisms. To determine the relative roles of transcriptional and posttranscriptional regulation, the effect of TNF on the turnover of thrombomodulin protein and mRNA was examined in human and bovine endothelial cells. Quantitative nuclease S1 protection assays showed a 70% to 90% reduction in thrombomodulin mRNA within 4 hours of the addition of 1.0 nmol/L TNF to the culture medium. The decrease in thrombomodulin mRNA resulted from inhibition of transcription, followed by rapid degradation of thrombomodulin transcripts (t1/2 less than or equal to 3 hours). In pulse-chase incubations, thrombomodulin synthesis decreased parallel with mRNA, but the rate of degradation of radiolabeled thrombomodulin was not significantly altered by TNF. Human thrombomodulin was degraded with a t1/2 of 8.2 +/- 2.4 hours (SD) or 7.5 +/- 1.3 hours (SD) in the absence or presence of TNF, respectively. We conclude that TNF acts primarily to inhibit thrombomodulin transcription. The subsequent decrease in activity results from the inherent instability of thrombomodulin mRNA and protein in these cells, and not from the regulation of thrombomodulin degradation.

scholarly journals The Extracellular Adherence Protein from Staphylococcus aureus Inhibits Neutrophil Binding to Endothelial Cells

2004 ◽  
Vol 72 (10) ◽  
pp. 6164-6167 ◽  
Author(s):  
Axana Haggar ◽  
Cecilia Ehrnfelt ◽  
Jan Holgersson ◽  
Jan-Ingmar Flock
Keyword(s):  
Staphylococcus Aureus ◽  
Endothelial Cells ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Neutrophil Adhesion ◽  
Necrosis Factor Alpha ◽  
Factor Alpha ◽  
Necrosis Factor ◽  
Adhesion Assays

ABSTRACT Extracellular adherence protein (Eap) from Staphylococcus aureus inhibits the adherence of neutrophils to nonstimulated and tumor necrosis factor alpha-stimulated endothelial cells in both static adhesion assays and flow adhesion assays. Consequently, Eap also impaired their transendothelial migration. During an S. aureus infection, Eap may thus serve to reduce inflammation by inhibiting neutrophil adhesion and extravasation.

scholarly journals Effects of Fluoroquinolones on the Migration of Human Phagocytes through Chlamydia pneumoniae-Infected and Tumor Necrosis Factor Alpha-Stimulated Endothelial Cells

2004 ◽  
Vol 48 (7) ◽  
pp. 2538-2543 ◽  
Author(s):  
Silvia M. Uriarte ◽  
Robert E. Molestina ◽  
Richard D. Miller ◽  
Jorge Bernabo ◽  
Alicia Farinati ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Chlamydia Pneumoniae ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Alpha ◽  
Necrosis Factor ◽  
Serial Dilutions

ABSTRACT The anti-inflammatory activities of three quinolones, levofloxacin, moxifloxacin, and gatifloxacin, were investigated with an in vitro model of transendothelial migration (TEM). Human umbilical vein endothelial cells (HUVEC) were seeded in Transwell inserts, treated with serial dilutions of antibiotics, infected with Chlamydia pneumoniae, or stimulated with tumor necrosis factor alpha (TNF-α). Neutrophils or monocytes were also preincubated with serial dilutions of each antibiotic. TEM was assessed by light microscopic examination of the underside of the polycarbonate membrane, and levels of interleukin-8 (IL-8) and monocyte chemotactic protein 1 (MCP-1) were measured by enzyme-linked immunosorbent assay. In HUVEC infected with C. pneumoniae or stimulated with TNF-α, all fluoroquinolones significantly decreased neutrophil and monocyte TEM, compared to antibiotic-free controls. Moxifloxacin and gatifloxacin produced a significant decrease in IL-8 in C. pneumoniae-infected and TNF-α-stimulated HUVEC; however, moxifloxacin was the only fluoroquinolone that produced a significant decrease in MCP-1 levels under both conditions. Results from this study indicate similarities in the anti-inflammatory activities of these fluoroquinolones, although no statistically significant decrease in chemokine secretion was observed when levofloxacin was used. Mechanisms of neutrophil and monocyte TEM inhibition by fluoroquinolone antibiotics are unknown but may be partially due to inhibition of IL-8 and MCP-1 production, respectively.

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