Granulocyte Macrophage Colony-stimulating Factor Augments ICAM-1 and VCAM-1 Activation of Eosinophil Function

Nagata, Michio; Sedgwick, Julie B.; Kita, Hirohito; Busse, William W.

doi:10.1165/ajrcmb.19.1.3001

Cited by 75 publications

(77 citation statements)

References 60 publications

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“…4b). The ability to induce eosinophil spontaneous adhesion is more potent with VCAM-1 than with ICAM-1 [28]. From this point of view, the current results demonstrated that the IFN-b-augmented adhesion of eosinophils to HUVECs was still observed following treatment with anti-b 2 integrin mAb.…”

Section: Ifn-b and Eosinophil-endothelial Cell Adhesionsupporting

confidence: 58%

Interferon- augments eosinophil adhesion-inducing activity of endothelial cells

Kobayashi

Takaku²,

Yokote³

et al. 2008

European Respiratory Journal

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Viral infections induce exacerbations of asthma. One of the earliest host responses to viral infections is the production of innate cytokines including type I interferons (IFNs), such as IFN-b, which may act to modify airway inflammation. The objective of the present study was to investigate whether IFN-b modifies the eosinophil adhesion-inducing activity of endothelial cells.Human umbilical vein endothelial cells (HUVECs) were stimulated with IFN-b for 24 h in the presence or absence of tumour necrosis factor (TNF)-a. Eosinophils were isolated from the peripheral blood of healthy volunteers. The ability of the IFN-b-stimulated HUVEC monolayers to induce eosinophil adhesion was assessed according to the eosinophil peroxidase assay.Eosinophil adhesion to HUVECs was significantly augmented by IFN-b in the presence of TNF-a but not in its absence. The augmented adhesion was inhibited by anti-a 4 integrin monoclonal antibody (mAb) or anti-b 2 integrin mAb. IFN-b significantly enhanced the expression of vascular cell adhesion molecule-1 and intercellular adhesion molecule-1 on HUVECs in the presence of TNF-a.Interferon-b can augment the adhesiveness of endothelial cells to eosinophils, mainly through the expression of vascular cell adhesion molecule-1 and intercellular adhesion molecule-1. This action of interferon-b may contribute to the intensification of airway inflammation in asthma that is associated with exacerbations induced by viral infections.

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Section: Ifn-b and Eosinophil-endothelial Cell Adhesionsupporting

confidence: 58%

Interferon- augments eosinophil adhesion-inducing activity of endothelial cells

Kobayashi

Takaku²,

Yokote³

et al. 2008

European Respiratory Journal

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“…1C). Chimeric CYBB mice received either eosinophils from BAL of OVAchallenged CD45.1 mice or eosinophils from the blood of IL-5 transgenic mice, since eosinophils from BAL can differ from blood eosinophils with regard to adhesion molecule expression and cell function (26,44,45). Eosinophils were isolated from the BAL of OVA-stimulated C57BL/6 mice that were prepared by challenging these mice with OVA 24 h before the OVA challenges in the chimeric mice as indicated in the timeline in Fig.…”

Section: Resultsmentioning

confidence: 99%

Nonhematopoietic NADPH oxidase regulation of lung eosinophilia and airway hyperresponsiveness in experimentally induced asthma

Abdala-Valencia

Earwood

Bansal

et al. 2007

American Journal of Physiology-Lung Cellular and Molecular Phys

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“…The importance of ICAM-1 for eosinophil functions other than locomotion was suggested in several reports. First, in GM-CSF-activated eosinophils, a blockade of ICAM-1 inhibited release of eosinophil-derived neurotoxin and superoxide production (17,40). Second, adherence of eosinophils to fibronectin, an ICAM-1-ligand, significantly up-regulated the release of cytotoxic mediators such as EDN, EPO, and leukotriene C 4 (4 -6, 15, 16), suggesting that cytokine-induced signaling and signaling from ICAM-1 do interact.…”

Section: Discussionmentioning

confidence: 99%

Cross-Talk between ICAM-1 and GM-CSF Receptor Signaling Modulates Eosinophil Survival and Activation

Pazdrak

Young

Stafford

et al. 2008

The Journal of Immunology

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Reversal of eosinophilic inflammation has been an elusive therapeutic goal in the management of asthma pathogenesis. In this regard, GM-CSF is a primary candidate cytokine regulating eosinophil activation and survival in the lung; however, its molecular mechanism of propagation and maintenance of stimulated eosinophil activation is not well understood. In this study, we elucidate those late interactions occurring between the GM-CSF receptor and activated eosinophil signaling molecules. Using coimmunoprecipitation with GM-CSF-stimulated eosinophils, we have identified that the GM-CSF receptor β-chain (GMRβ) interacted with ICAM-1 and Shp2 phosphatase, as well as Slp76 and ADAP adaptor proteins. Separate experiments using affinity binding with a tyrosine-phosphorylated peptide containing an ITIM (ICAM-1 residues 480–488) showed binding to Shp2 phosphatase and GMRβ. However, the interaction of GMRβ with the phosphorylated ICAM-1-derived peptide was observed only with stimulated eosinophil lysates, suggesting that the interaction of GMRβ with ICAM-1 required phosphorylated Shp2 and/or phosphorylated GMRβ. Importantly, we found that inhibition of ICAM-1 in activated eosinophils blocked GM-CSF-induced expression of c-fos, c-myc, IL-8, and TNF-α. Moreover, inhibition of ICAM-1 expression with either antisense oligonucleotide or an ICAM-1-blocking Ab effectively inhibited ERK activation and eosinophil survival. We concluded that the interaction between ICAM-1 and the GM-CSF receptor was essential for GM-CSF-induced eosinophil activation and survival. Taken together, these results provide novel mechanistic insights defining the interaction between ICAM-1 and the GM-CSF receptor and highlight the importance of targeting ICAM-1 and GM-CSF/IL-5/IL-3 receptor systems as a therapeutic strategy to counter eosinophilia in asthma.

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Granulocyte Macrophage Colony-stimulating Factor Augments ICAM-1 and VCAM-1 Activation of Eosinophil Function

Cited by 75 publications

References 60 publications

Interferon- augments eosinophil adhesion-inducing activity of endothelial cells

Interferon- augments eosinophil adhesion-inducing activity of endothelial cells

Nonhematopoietic NADPH oxidase regulation of lung eosinophilia and airway hyperresponsiveness in experimentally induced asthma

Cross-Talk between ICAM-1 and GM-CSF Receptor Signaling Modulates Eosinophil Survival and Activation

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