Vascular Cell Adhesion Molecule-1 and Eosinophil Adhesion to Cultured Human Umbilical Vein Endothelial Cells <i>In Vitro</i>

Kyan-Aung, U; Haskard, Dorian O.; Lee, Tak H.

doi:10.1165/ajrcmb/5.5.445

Cited by 42 publications

(17 citation statements)

References 25 publications

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“…However, TNF-α’s role as a proinflammatory cytokine in supporting tissue eosinophilia is unlikely to be through direct chemotactic effects. TNF-α, in contrast to GM-CSF, has been shown to play a critical role in endothelial events necessary for granulocyte transendothelial migration [18, 23, 24, 25, 26, 27]. Thus, our findings that TNF-α pretreatment of an endothelial monolayer could support GM-CSF-induced eosinophil transendothelial migration are consistent with previous observations about the biologic role of TNF-α.…”

Section: Discussionsupporting

confidence: 93%

See 1 more Smart Citation

Tumor Necrosis Factor α Is Necessary for Granulocyte-Macrophage-Colony-Stimulating-Factor-Induced Eosinophil Transendothelial Migration

Erger

Casale²

1997

Int Arch Allergy Immunol

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Background: We have previously shown that granulocyte macrophage-colony stimulating factor (GM-CSF) was capable of inducing eosinophil migration across naked filters but not endothelial monolayers. Tumor necrosis factor α (TNF-α) has been shown to be a key factor in granulocyte adhesion and transendothelial migration. Methods: We, therefore, pretreated human umbilical vein endothelial cell (HUVEC) monolayers with TNF-α and studied whether TNF-α could support GM-CSF-induced eosinophil transendothelial migration. Results: We found that TNF-α supported GM-CSF-induced eosinophil transendothelial migration and that this process was: (1) dependent upon GM-CSF and TNF-α dose; (2) time-dependent; (3) not due to TNF-α having a chemotactic effect itself; (4) not due to TNF-α-induced soluble factor production by endothelium, and (5) inhibitable by actinomycin D. We next studied the specificity of this response. Neutrophils did not migrate across TNF-α-pretreated endothelium in response to GM-CSF. TNF-α pretreatment of A549 human type-II-like epithelial lung cells (A549) did not support GM-CSF-induced transepithelial migration. Neither interleukin (IL)-1 nor GM-CSF pretreatment of the HUVEC supported GM-CSF-induced transendothelial migration. However, IL-5 induced eosinophil migration through naked filters as well as TNF-α-pretreated HUVEC in a manner analogous to GM-CSF. Antibodies to ICAM-1, but not VCAM-1 significantly inhibited this response. Although IL-1 did not support GM-CSF-induced eosinophil transendothelial migration, IL-1 and TNF-α induced equivalent expression of ICAM-1 on HUVEC. Conclusion: Thus, TNF-α-supported eosinophil transendothelial migration in response to GM-CSF (and IL-5) is dependent upon ICAM-1, and is both specific and complex.

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Section: Discussionsupporting

confidence: 93%

“…TNF-α has been shown to upregulate critical adhesion molecules [11, 24, 25, 26, 27] and induce microvascular permeability [28] and mucus release [29]. In addition, both TNF-α and GM-CSF have been shown to be involved in airway hyperresponsiveness [5, 30] and the release of additional mediators and cytokines from a variety of cells [5, 18].…”

Section: Discussionmentioning

confidence: 99%

Tumor Necrosis Factor α Is Necessary for Granulocyte-Macrophage-Colony-Stimulating-Factor-Induced Eosinophil Transendothelial Migration

Erger

Casale²

1997

Int Arch Allergy Immunol

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“…This finding reveals a newly identified activity for mOSM on lung fibroblasts and indicates a potential additional mechanism in eosinophil accumulation in the lung parenchyma. VLA-4 (␣ 4 ␤ 1 /CD49d/ CD29 integrin), a receptor for VCAM-1, is expressed on eosinophils (5)(6)(7)(8). VCAM-1/VLA-4 binding has been shown to be important in OVA allergen-induced eosinophil infiltration into the lung (9, 10) and eotaxin-induced eosinophil migration into tissue (11,12).…”

Section: Discussionmentioning

confidence: 99%

“…Eosinophils have been shown to express VLA-4 (␣ 4 ␤ 1 / CD49d/CD29 integrin) which binds VCAM-1 in vitro (5)(6)(7)(8). The importance of these interactions has been demonstrated in studies where in vivo blockade of VCAM-1/VLA-4 inhibited OVA allergen-induced eosinophil infiltration into the lung (9, 10) and eotaxin-induced eosinophil adhesion and transendothelial migration into tissue (11,12).…”

Section: Oncostatin-m Up-regulates Vcam-1 and Synergizes With Il-4 Inmentioning

confidence: 99%

Oncostatin-M Up-Regulates VCAM-1 and Synergizes with IL-4 in Eotaxin Expression: Involvement of STAT6

Fritz

Kerr

et al. 2006

The Journal of Immunology

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Oncostatin-M (OSM) is an IL-6/gp130 family member that can stimulate the eosinophil-selective CC chemokine eotaxin-1 in vitro and eosinophil accumulation in mouse lung in vivo. The adhesion molecule VCAM-1 and eotaxin have been implicated in extravasation and accumulation of eosinophils into tissue in animal models of asthma. In this study, we investigated the role of OSM in regulation of VCAM-1 expression, and STAT6 tyrosine 641 phosphorylation in murine fibroblasts. OSM induced VCAM-1 expression in C57BL/6 mouse lung fibroblasts (MLF) and NIH 3T3 fibroblasts at the protein and mRNA level in vitro. OSM also induced STAT6 Y641 phosphorylation in MLF and NIH 3T3 fibroblasts, an activity not observed with other IL-6/gp130 cytokine family members (IL-6, leukemia inhibitory factor, cardiotropin-1, and IL-11) nor in cells derived from STAT6−/− mice (STAT6−/− MLF). STAT6 was not essential for OSM-induced VCAM-1 or eotaxin-1 as assessed in STAT6−/− MLF. Combination of IL-4 and OSM synergistically enhanced eotaxin-1 expression in MLF. IL-4 induction and the IL-4/OSM synergistic induction of eotaxin-1 was abrogated in STAT6−/− MLF, however, regulation of IL-6 was similar in −/− or wild-type MLF. Induction of VCAM-1 by OSM was diminished by pharmacological inhibitors of PI3K (LY294002) but not inhibitors of ERK1/2 (PD98059) or p38 MAPK (SB203580). These data support the role of OSM in eosinophil accumulation into lung tissue through eotaxin-1 and VCAM-1 expression and the notion that OSM is able to induce unique signal transduction events through its receptor complex of OSMR β-chain and gp130.

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“…For instance, blood eosinophils stimulated in vitro with IL-5, PAF or fMLP achieved similar levels of CD11b and VLA-4 expression as BAL eosinophils obtained 18 h post-challenge [20,138,[141][142][143][144]. The stimuli also caused a decrease in L-selectin expression in eosinophils.…”

Section: Phenotypical Heterogeneitymentioning

confidence: 99%

Pulmonary immune cells in health and disease: the eosinophil leucocyte (Part I)

Kroegel¹,

Virchow²,

Luttmann³

et al. 1994

Eur Respir J

129

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P Pu ul lm mo on na ar ry y i im mm mu un ne e c ce el ll ls s i in n h he ea al lt th h a an nd d d di is se ea as se e: : t th he e e eo os si in no op ph hi il l l le eu uc co oc cy yt te e ( (P Pa ar rt t I I) ) ABSTRACT: Increasing evidence has accumulated to suggest that eosinophils play a key role in the pathogenesis of asthma and other pulmonary diseases by damaging infiltrated bronchial tissue and lung parenchyma. The first part of this review on eosinophils describes the cellular characteristics and properties of the cell, which help in understanding its role in disease. The article focuses on origin, maturation and differentiation of the eosinophil, its morphological and phenotypical properties, as well as its preformed and newly generated mediators of inflammation. The cause and putative significance of eosinophil heterogeneity in respect to function and density will also be discussed. In addition, the naturally occurring mediators through which eosinophils are activated and communicate with other inflammatory cells are outlined.The first part closes with new aspects of eosinophil recruitment from the circulation into perivascular tissue, including nonselective and putative selective adhesion mechanisms and chemotaxis.

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Vascular Cell Adhesion Molecule-1 and Eosinophil Adhesion to Cultured Human Umbilical Vein Endothelial Cells In Vitro

Cited by 42 publications

References 25 publications

Tumor Necrosis Factor α Is Necessary for Granulocyte-Macrophage-Colony-Stimulating-Factor-Induced Eosinophil Transendothelial Migration

Tumor Necrosis Factor α Is Necessary for Granulocyte-Macrophage-Colony-Stimulating-Factor-Induced Eosinophil Transendothelial Migration

Oncostatin-M Up-Regulates VCAM-1 and Synergizes with IL-4 in Eotaxin Expression: Involvement of STAT6

Pulmonary immune cells in health and disease: the eosinophil leucocyte (Part I)

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