Increased expression of endothelial cell adhesion molecules due to mediator release from human foreskin mast cells stimulated by autoantibodies in chronic urticaria sera

Hoon Lee Kwang, Young Kim Ji, Dong Seung Kang, Jean Choi Yoo, Won Jae Lee, Youl Ro Jai

Research output: Contribution to journalArticle

25 Citations (Scopus)

Abstract

Histamine-releasing antibodies that act against the epitope of the α chain of FcεRI (anti-FcεRIα antibody) that may affect pathogenesis in serum of patients with chronic urticaria. We assessed the capability of anti-FcεRIα antibody in sera from patients with chronic urticaria to release histamine and cytokines, and to induce the expression of endothelial cell adhesion molecules. We also assessed the release of inflammatory mediators from cultured foreskin mast cells, and expression of endothelial cell adhesion molecules on human dermal microvascular endothelial cells. Cells were pretreated with mast cell-conditioned media: Culture media of mast cells treated with sera from chronic urticaria patients containing anti-FcεRIα antibody. Histamine release from human foreskin mast cells challenged with sera, increased after both 20 min and 16 h intervals. Leukotriene D 4 release also increased at both 20 min and 16 h. Tumor necrosis factor-α increased significantly in foreskin mast cell culture challenged with sera of chronic urticaria patients. After the stimulation of human dermal microvascular endothelial cells with the conditioned media, the expression of intercellular cell adhesion molecule-1, vascular cell adhesion molecule-1, and E-selectin increased significantly. Treatment of the conditioned media with anti-tumor necrosis factor-α monoclonal antibody partially inhibited the expression of intercellular cell adhesion molecule-1, vascular cell adhesion molecule-1, and E-selectin. The data suggest that sera from patients with chronic urticaria containing anti-FcεRIα antibody release mediators and tumor necrosis factor-α by activating human foreskin mast cells. This release can play a pathogenic role in chronic urticaria by activating endothelial cells, in part due to the actions of tumor necrosis factor-α from mast cells.

Original languageEnglish
Pages (from-to)658-663
Number of pages6
JournalJournal of Investigative Dermatology
Volume118
Issue number4
DOIs
Publication statusPublished - 2002 Apr

Fingerprint

Foreskin
Endothelial cells
Urticaria
Cell Adhesion Molecules
Mast Cells
Autoantibodies
Endothelial Cells
Tumor Necrosis Factor-alpha
Antibodies
Histamine
Serum
Anti-Idiotypic Antibodies
E-Selectin
Vascular Cell Adhesion Molecule-1
Cell adhesion
Conditioned Culture Medium
Histamine Release
Intercellular Adhesion Molecule-1
Leukotriene D4
Molecules

All Science Journal Classification (ASJC) codes

  • Biochemistry
  • Molecular Biology
  • Dermatology
  • Cell Biology

Cite this

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title = "Increased expression of endothelial cell adhesion molecules due to mediator release from human foreskin mast cells stimulated by autoantibodies in chronic urticaria sera",
abstract = "Histamine-releasing antibodies that act against the epitope of the α chain of FcεRI (anti-FcεRIα antibody) that may affect pathogenesis in serum of patients with chronic urticaria. We assessed the capability of anti-FcεRIα antibody in sera from patients with chronic urticaria to release histamine and cytokines, and to induce the expression of endothelial cell adhesion molecules. We also assessed the release of inflammatory mediators from cultured foreskin mast cells, and expression of endothelial cell adhesion molecules on human dermal microvascular endothelial cells. Cells were pretreated with mast cell-conditioned media: Culture media of mast cells treated with sera from chronic urticaria patients containing anti-FcεRIα antibody. Histamine release from human foreskin mast cells challenged with sera, increased after both 20 min and 16 h intervals. Leukotriene D 4 release also increased at both 20 min and 16 h. Tumor necrosis factor-α increased significantly in foreskin mast cell culture challenged with sera of chronic urticaria patients. After the stimulation of human dermal microvascular endothelial cells with the conditioned media, the expression of intercellular cell adhesion molecule-1, vascular cell adhesion molecule-1, and E-selectin increased significantly. Treatment of the conditioned media with anti-tumor necrosis factor-α monoclonal antibody partially inhibited the expression of intercellular cell adhesion molecule-1, vascular cell adhesion molecule-1, and E-selectin. The data suggest that sera from patients with chronic urticaria containing anti-FcεRIα antibody release mediators and tumor necrosis factor-α by activating human foreskin mast cells. This release can play a pathogenic role in chronic urticaria by activating endothelial cells, in part due to the actions of tumor necrosis factor-α from mast cells.",
author = "Kwang, {Hoon Lee} and Ji, {Young Kim} and Kang, {Dong Seung} and Yoo, {Jean Choi} and Lee, {Won Jae} and Jai, {Youl Ro}",
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Increased expression of endothelial cell adhesion molecules due to mediator release from human foreskin mast cells stimulated by autoantibodies in chronic urticaria sera. / Kwang, Hoon Lee; Ji, Young Kim; Kang, Dong Seung; Yoo, Jean Choi; Lee, Won Jae; Jai, Youl Ro.

In: Journal of Investigative Dermatology, Vol. 118, No. 4, 04.2002, p. 658-663.

Research output: Contribution to journalArticle

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AU - Kwang, Hoon Lee

AU - Ji, Young Kim

AU - Kang, Dong Seung

AU - Yoo, Jean Choi

AU - Lee, Won Jae

AU - Jai, Youl Ro

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N2 - Histamine-releasing antibodies that act against the epitope of the α chain of FcεRI (anti-FcεRIα antibody) that may affect pathogenesis in serum of patients with chronic urticaria. We assessed the capability of anti-FcεRIα antibody in sera from patients with chronic urticaria to release histamine and cytokines, and to induce the expression of endothelial cell adhesion molecules. We also assessed the release of inflammatory mediators from cultured foreskin mast cells, and expression of endothelial cell adhesion molecules on human dermal microvascular endothelial cells. Cells were pretreated with mast cell-conditioned media: Culture media of mast cells treated with sera from chronic urticaria patients containing anti-FcεRIα antibody. Histamine release from human foreskin mast cells challenged with sera, increased after both 20 min and 16 h intervals. Leukotriene D 4 release also increased at both 20 min and 16 h. Tumor necrosis factor-α increased significantly in foreskin mast cell culture challenged with sera of chronic urticaria patients. After the stimulation of human dermal microvascular endothelial cells with the conditioned media, the expression of intercellular cell adhesion molecule-1, vascular cell adhesion molecule-1, and E-selectin increased significantly. Treatment of the conditioned media with anti-tumor necrosis factor-α monoclonal antibody partially inhibited the expression of intercellular cell adhesion molecule-1, vascular cell adhesion molecule-1, and E-selectin. The data suggest that sera from patients with chronic urticaria containing anti-FcεRIα antibody release mediators and tumor necrosis factor-α by activating human foreskin mast cells. This release can play a pathogenic role in chronic urticaria by activating endothelial cells, in part due to the actions of tumor necrosis factor-α from mast cells.

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