Expression of Adhesion Molecules in Cultured Human Nasal Mucosal Microvascular Endothelial Cells Activated by Interleukin–1â or Tumor Necrosis Factor–·: Effects of Dexamethasone

Abstract

Adhesion molecules of microvascular endothelial cells play a key role in the inflammatory processes involved in nonallergic sinusitis. We investigated the cytokine–regulated expression of intercellular adhesion molecule–1 (ICAM–1), E–selectin and vascular cell adhesion molecule–1 (VCAM–1), and the effect of dexamethasone on these expressions in cultured human nasal microvascular endothelial cells (HNMEC). ICAM–1 was enhanced, and E–selectin and VCAM–1 were induced in a dose–dependent fashion following stimulation with IL–1β or TNF–α. HNMEC differed from human umbilical vein endothelila cells in that (1) maximal upregulation of ICAM–1 expression induced by IL–1β or TNF–α required more time (2) TNF–α was more potent than IL–1β in VCAM–1 expression, and (3) dexamethasone inhibited the upregulation of E–selectin expression alone. These findings contribute to a better understanding of the characteristic features of leukocyte infiltration into inflamed tissue and the effect of glucocorticoid in nonallergic chronic sinusitis.

Mechanisms and clinical implications of glucocorticosteroids in the treatment of allergic rhinitis

“…GC down-regulates nasal fibroblast functions, including basic fibroblast growth factor (bFGF)-induced proliferation, TNF-a-induced ICAM-1 expression, TNF-a-or IL-4-stimulated eotaxin release [56], TNF-a-induced matrix metalloproteinase production [57] and TNF-a-induced vascular endothelial growth factor (VEGF) and bFGF production [58]. GC inhibits TNF-a-or IL-1b-stimulated E-selectin expression on nasal vascular endothelial cells [59]. The effect of GC on vascular cel adhesion molecule 1 (VCAM-1) expression on nasal vascular endothelial cells is controversial [60,61].…”

Heterogeneity of Human Nasal Vascular and Sinusoidal Endothelial Cells from the Inferior Turbinate

“…In conclusion, we describe a simple and novel protocol for the isolation and cultivation of two heterogeneous populations of HNMEC that will be of great advantage for in vitro research in illnesses such as asthma, non-allergic inflammation, hyperreactivity, allergic rhinitis (22,23), vasculitides such as Wegener's granulomatosis (24), and other nasal diseases. The use of these two distinct, well-characterized populations of HNMEC as targets in such studies may provide important clinical knowledge regarding the role of each EC type to respond during inflammation and various types of damage in nasal disorders.…”

Wirkmechanismen nasaler Glukokortikosteroide in der Therapie der allergischen Rhinitis

“…Darüber hinaus wird die durch TNF-α-induzierte Produktion von Matrixmetalloproteinasen [57] und die ebenfalls TNF-α-induzierte Produktion von "vascular endothelial growth factor" (VEGF) und bFGF vermindert [58]. GC hemmen außerdem die durch TNF-α-oder IL-1β-stimulierte E-Selektin-Expression auf nasalen, vaskulären Endothelzellen [59]. Der Effekt von GC auf die Expression des vaskulären Zelladhäsionsmoleküls 1 (VCAM-1) wird kontrovers diskutiert [60,61].…”