Soluble vascular cell adhesion molecule‐1 induces human eosinophil migration

Ueki, Shigeharu; Kihara, Junko; Kato, Hikari; Ito, Wataru; Takeda, Masahide; Kobayashi, Yoshimi; Kayaba, Hiroyuki; Chihara, Junichi

doi:10.1111/j.1398-9995.2008.01871.x

Cited by 23 publications

(22 citation statements)

References 31 publications

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“…Moreover, the level of sVCAM-1 was strongly reduced in the BALF of P2Y 2 -deficient mice. Interestingly, sVCAM-1 was described recently as an inducer of eosinophil chemotaxis (19). Allergen-induced accumulation of eosinophils was previously associated with increased levels of sVCAM-1 (20).…”

Section: Discussionmentioning

confidence: 96%

P2Y2 Receptor Regulates VCAM-1 Membrane and Soluble Forms and Eosinophil Accumulation during Lung Inflammation

Vanderstocken

Bondue

Horckmans

et al. 2010

The Journal of Immunology

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ATP has been defined as a key mediator of asthma. In this study, we evaluated lung inflammation in mice deficient for the P2Y2 purinergic receptor. We observed that eosinophil accumulation, a distinctive feature of lung allergic inflammation, was defective in OVA-treated P2Y2-deficient mice compared with OVA-treated wild type animals. Interestingly, the upregulation of VCAM-1 was lower on lung endothelial cells of OVA-treated P2Y2−/− mice compared with OVA-treated wild type animals. Adhesion assays demonstrated that the action of UTP on leukocyte adhesion through the regulation of endothelial VCAM-1 was abolished in P2Y2-deficient lung endothelial cells. Additionally, the level of soluble VCAM-1, reported as an inducer of eosinophil chemotaxis, was strongly reduced in the bronchoalveolar lavage fluid (BALF) of P2Y2-deficient mice. In contrast, we observed comparable infiltration of macrophages and neutrophils in the BALF of LPS-aerosolized P2Y2+/+ and P2Y2−/− mice. This difference could be related to the much lower level of ATP in the BALF of LPS-treated mice compared with OVA-treated mice. Our data define P2Y2 as a regulator of membrane and soluble forms of VCAM-1 and eosinophil accumulation during lung inflammation.

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Section: Discussionmentioning

confidence: 96%

P2Y2 Receptor Regulates VCAM-1 Membrane and Soluble Forms and Eosinophil Accumulation during Lung Inflammation

Vanderstocken

Bondue

Horckmans

et al. 2010

The Journal of Immunology

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“…Informed consent was obtained from each subject, and the study protocols were approved by the Ethics Committee of Akita University School of Medicine. Cells were isolated as previously described [21][22][23][24][25][26]. In brief, granulocytes were isolated by sedimentation with 6% dextran followed by centrifugation on 1.088 Percoll (Pharmacia, Uppsala, Sweden) density gradients.…”

Section: Cell Preparationmentioning

confidence: 99%

“…Chemotaxis of eosinophils was conducted in duplicate using 5-mm-pore polycarbonate, polyvinylpyrrolidone-free membranes in Boyden chambers [21,22,26]. Aliquots of 100 mL of the cell suspension at 0.5 Â 10 6 cells/mL were placed in the upper chambers.…”

Section: Chemotaxis Assaymentioning

confidence: 99%

Adiponectin attenuates human eosinophil adhesion and chemotaxis: implications in allergic inflammation

et al. 2013

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“…A panel of phosphoproteins was measured in duplicate using a bead-based multiplex assay (Bio-Plex phosphoprotein assay; Bio-Rad) [19], according to the manufacturer’s instructions. To study the leptin-induced MAPK signaling pathway, purified eosinophils (0.5 × 10 6 cells) were incubated with leptin (10 –6 g/ml) for the indicated time.…”

Section: Methodsmentioning

confidence: 99%

Leptin Has a Priming Effect on Eotaxin-Induced Human Eosinophil Chemotaxis

Kato

Ueki

Kamada

et al. 2011

Int Arch Allergy Immunol

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Background: Tissue eosinophilia is one of the hallmarks of allergic diseases and Th2-type immune responses including asthma. Systemic inflammation caused by adipose tissue in obesity via production of adipokines such as leptin has been attracting attention recently as a contributor to exacerbation of allergic immune reactions. In this study, we examined whether leptin might affect eosinophil chemotactic responses. Methods: Peripheral blood eosinophils were purified, and the effect of leptin on eosinophil migration was investigated using in vitro systems. Results: High concentrations of leptin induced eosinophil chemotaxis and rapid phosphorylation of ERK1/2 and p38 mitogen-activated protein kinase but not calcium mobilization. We also found that pretreatment of eosinophils with physiological concentrations of leptin amplified the chemotactic responses to eotaxin. This leptin-primed chemotaxis appears to be associated with increased calcium mobilization but not with ERK1/2 and p38 pathways. Conclusions: These results indicate that leptin has both direct and indirect effects on eosinophil chemotaxis and intracellular signaling. In physiological settings, leptin may maintain eosinophil accumulation at allergic inflammatory foci.

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Soluble vascular cell adhesion molecule‐1 induces human eosinophil migration

Abstract: Our results raise the possibility of sVCAM-1 in the fluid phase as a significant contributor to the heightened eosinophilic inflammatory response.

Cited by 23 publications

References 31 publications

P2Y2 Receptor Regulates VCAM-1 Membrane and Soluble Forms and Eosinophil Accumulation during Lung Inflammation

P2Y2 Receptor Regulates VCAM-1 Membrane and Soluble Forms and Eosinophil Accumulation during Lung Inflammation

Adiponectin attenuates human eosinophil adhesion and chemotaxis: implications in allergic inflammation

Leptin Has a Priming Effect on Eotaxin-Induced Human Eosinophil Chemotaxis

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