scholarly journals Helicobacter pylori-Induced Activation of Human Endothelial Cells

2002 ◽  
Vol 70 (8) ◽  
pp. 4581-4590 ◽  
Author(s):  
M. Innocenti ◽  
A.-C. Thoreson ◽  
R. L. Ferrero ◽  
E. Strömberg ◽  
I. Bölin ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Helicobacter Pylori ◽  
Gastric Mucosa ◽  
Adhesion Molecule ◽  
Cell Activation ◽  
Ulcer Formation ◽  
Blood Group Antigens ◽  
Adhesion Molecule Expression ◽  
Human Endothelial Cells ◽  
H Pylori

ABSTRACT Helicobacter pylori infection causes active chronic inflammation with a continuous recruitment of neutrophils to the inflamed gastric mucosa. To evaluate the role of endothelial cells in this process, we have examined adhesion molecule expression and chemokine and cytokine production from human umbilical vein endothelial cells stimulated with well-characterized H. pylori strains as well as purified proteins. Our results indicate that endothelial cells actively contribute to neutrophil recruitment, since stimulation with H. pylori bacteria induced upregulation of the adhesion molecules VCAM-1, ICAM-1, and E-selectin as well as the chemokines interleukin 8 (IL-8) and growth-related oncogene alpha (GRO-α) and the cytokine IL-6. However, there were large variations in the ability of the different H. pylori strains to stimulate endothelial cells. These interstrain variations were seen irrespective of whether the strains had been isolated from patients with duodenal ulcer disease or asymptomatic carriers and were not solely related to the expression of known virulence factors, such as the cytotoxin-associated gene pathogenicity island, vacuolating toxin A, and Lewis blood group antigens. In addition, one or several unidentified proteins which act via NF-κB activation seem to induce endothelial cell activation. In conclusion, human endothelial cells produce neutrophil-recruiting factors and show increased adhesion molecule expression after stimulation with certain H. pylori strains. These effects probably contribute to the continuous recruitment of neutrophils to H. pylori-infected gastric mucosa and may also contribute to tissue damage and ulcer formation.

scholarly journals Direct Activation of Human Endothelial Cells by Plasmodium falciparum-Infected Erythrocytes

2005 ◽  
Vol 73 (6) ◽  
pp. 3271-3277 ◽  
Author(s):  
Nicola K. Viebig ◽  
Ulrich Wulbrand ◽  
Reinhold Förster ◽  
Katherine T. Andrews ◽  
Michael Lanzer ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Plasmodium Falciparum ◽  
Endothelial Cell ◽  
Adhesion Molecule ◽  
Cell Activation ◽  
Physical Contact ◽  
Intercellular Adhesion Molecule ◽  
Immune Reactivity ◽  
Human Endothelial Cells ◽  
Tnf Α

ABSTRACT Cytoadherence of Plasmodium falciparum-infected erythrocytes (PRBC) to endothelial cells causes severe clinical disease, presumably as a of result perfusion failure and tissue hypoxia. Cytoadherence to endothelial cells is increased by endothelial cell activation, which is believed to occur in a paracrine fashion by mediators such as tumor necrosis factor alpha (TNF-α) released from macrophages that initially recognize PRBC. Here we provide evidence that PRBC directly stimulate human endothelial cells in the absence of macrophages, leading to increased expression of adhesion-promoting molecules, such as intercellular adhesion molecule 1. Endothelial cell stimulation by PRBC required direct physical contact for a short time (30 to 60 min) and was correlated with parasitemia. Gene expression profiling of endothelial cells stimulated by PRBC revealed increased expression levels of chemokine and adhesion molecule genes. PRBC-stimulated endothelial cells especially showed increased expression of molecules involved in parasite adhesion but failed to express molecules promoting leukocyte adhesion, such as E-selectin and vascular cell adhesion molecule 1, even after challenge with TNF-α. Collectively, our data suggest that stimulation of endothelial cells by PRBC may have two effects: prevention of parasite clearance through increased cytoadherence and attenuation of leukocyte binding to endothelial cells, thereby preventing deleterious immune reactivity.

Effects of Aminoguanidine on Adhesion Molecule Expression of Human Endothelial Cells

Pharmacology ◽  
1997 ◽  
Vol 55 (3) ◽  
pp. 126-135 ◽  
Author(s):  
EJ. Menzel ◽  
J. Neumüller ◽  
G. Sengoelge ◽  
R. Reihsner
Keyword(s):  
Endothelial Cells ◽  
Adhesion Molecule ◽  
Adhesion Molecule Expression ◽  
Human Endothelial Cells

scholarly journals Selective Upregulation of Endothelial E-Selectin in Response to Helicobacter pylori-Induced Gastritis

2009 ◽  
Vol 77 (7) ◽  
pp. 3109-3116 ◽  
Author(s):  
Helena Svensson ◽  
Malin Hansson ◽  
Jan Kilhamn ◽  
Steffen Backert ◽  
Marianne Quiding-Järbrink
Keyword(s):  
Helicobacter Pylori ◽  
Gastric Mucosa ◽  
Adhesion Molecules ◽  
Adhesion Molecule ◽  
Adhesion Protein ◽  
Type Iv ◽  
Endothelial Adhesion Molecules ◽  
H Pylori ◽  
Vascular Adhesion

ABSTRACT Helicobacter pylori is one of the most common bacterial pathogens, infecting up to 50% of the world's population. The host is not able to clear the infection, leading to life-long chronic inflammation with continuous infiltration of lymphocytes and granulocytes. The migration of leukocytes from the blood into inflamed tissue is dependent on adhesion molecules expressed on the vascular endothelium. The aim of this study was to characterize the effect of H. pylori-induced gastritis with regard to the expression of endothelial adhesion molecules in the gastric mucosa and compare this to other types of chronic mucosal inflammations. Our results demonstrate an increased level of expression of the adhesion molecule E-selectin, but not of intracellular adhesion molecule 1, vascular adhesion molecule 1, or vascular adhesion protein 1, in H. pylori-induced gastritis but not in gastritis induced by acetylsalicylic acid or pouchitis. The upregulated E-selectin expression was determined to be localized to the gastric mucosa rather than being a systemic response to the infection. Moreover, the H. pylori type IV secretion system encoded by the cag pathogenicity island (cagPAI) was found to be an important determinant for the upregulation of human endothelial E-selectin expression in vitro, and this process is probably dependent on the CagL protein, mediating binding to α5β1 integrins. Thus, endothelial E-selectin expression induced by H. pylori probably contributes to the large influx of neutrophils and macrophages seen in infected individuals, and our results suggest that this process may be more pronounced in patients infected with cagPAI-positive H. pylori strains and may thereby contribute to tissue damage in these individuals.

Dextromethorphan Attenuates LPS-Induced Adhesion Molecule Expression in Human Endothelial Cells

2013 ◽  
Vol 20 (2) ◽  
pp. 190-201 ◽  
Author(s):  
Shinn-Jong Jiang ◽  
Sheng-Yao Hsu ◽  
Chuan-Rou Deng ◽  
Huey-Chun Huang ◽  
Shu-Lin Liu ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Adhesion Molecule ◽  
Adhesion Molecule Expression ◽  
Human Endothelial Cells
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