Endothelial cells modulate eosinophil surface markers and mediator release

Mj, Dallaire; Ferland, Claudine; Pagé, Nathalie; Lavigne, Sophie; Davoine, Francis; Laviolette, Michel

doi:10.1183/09031936.03.00102002

Cited by 42 publications

(37 citation statements)

References 46 publications

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“…51 53 This may be due to a redundancy in function of MMPs. Redundancy of MMP activity for neovascularization and hematopoietic stem cell mobilization was recently demonstrated in vivo by using MMP-9 knockout (KO) mice, MMP-2 KO mice, and double KOs.…”

Section: Discussionmentioning

confidence: 99%

Vascular cell adhesion molecule 1 (VCAM-1) activation of endothelial cell matrix metalloproteinases: role of reactive oxygen species

Deem

Cook‐Mills

2004

Blood

174

209

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Lymphocytes bound at endothelial cell junctions extravasate within minutes. Lymphocyte-endothelial cell binding is mediated by receptors such as vascular cell adhesion molecule 1 (VCAM-1). VCAM-1 activates endothelial cell nicotinamide adenine dinucleotide phosphate (NADPH) oxidase in minutes, and this activity is required for VCAM-1-dependent lymphocyte migration. In this report, we examined mechanisms for activation of matrix metalloproteinases (MMPs) during VCAM-1-dependent lymphocyte migration. Lymphocyte binding to VCAM-1 rapidly activated endothelial cell-associ- IntroductionLymphocytes migrate out of the blood between endothelial cells and into tissues where the lymphocytes can interact with antigen. Endothelial cells bind lymphocytes through cell surface adhesion molecules. One of these adhesion molecules is vascular cell adhesion molecule 1 (VCAM-1). It is important to understand VCAM-1 signaling because it is involved in several diseases. For example, VCAM-1 is required for eosinophil infiltration into the lung in experimental ovalbumin-induced asthma, 1 as well as T-cell infiltration across the blood-brain barrier in experimental allergic encephalomyelitis (EAE). 2 In addition, VCAM-1 functions in combination with other adhesion molecules during chronic inflammation and tumor metastasis. Understanding VCAM-1 signaling may have important implications for disease intervention.We have reported that VCAM-1 signaling in endothelial cells is required for VCAM-1-dependent lymphocyte migration. 3 Stimulation of VCAM-1 activates endothelial cell nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, which catalyzes the release of low levels of reactive oxygen species (ROS) in cytokinetreated human umbilical vein endothelial cells (HUVECs) and in endothelial cell lines. 4,5 These ROS are required for VCAM-1-stimulated endothelial cell actin restructuring and lymphocyte migration. 3,6,7 Therefore, ROS are involved in modulating endothelial cell function to promote VCAM-1-dependent lymphocyte migration.It has been reported that VCAM-1-dependent adhesion of a T-cell line activates lymphocyte matrix metalloproteinases (MMPs) after 5 hours. 8 However, the mechanism(s) for VCAM-1 activation of lymphocyte MMPs is not known. It is also not known whether VCAM-1 signaling activates endothelial cell MMPs. Activated MMPs degrade extracellular matrix, cell surface receptors in cell-cell junctions, and tight junction proteins. 9-11 MMP activation can be regulated by ROS. In smooth muscle cells, the latent form of MMP-2 (pro-MMP-2) is released after mechanical stretchstimulated production of ROS by NADPH oxidase. 12 In cell-free systems, low concentrations of ROS can activate pro-MMPs by oxidation of the sulfide bond in the prodomain of the MMP followed by release of this prodomain by autocatalytic cleavage. 13 In this report, we demonstrate that VCAM-1 rapidly activates endothelial cell-associated MMPs and that this activation is mediated by endothelial cell-derived ROS. In addition, endothelial cell-derived ROS are i...

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Section: Discussionmentioning

confidence: 99%

Vascular cell adhesion molecule 1 (VCAM-1) activation of endothelial cell matrix metalloproteinases: role of reactive oxygen species

Deem

Cook‐Mills

2004

Blood

174

209

View full text Add to dashboard Cite

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“…CD11b/CD18 can also mediate a constitutive low-level adhesion of VCAM-1 and supports adhesion and transmigration together with a4b1 [40]. Interaction of CD11b with its ligands on endothelial cells can also induce activation of eosinophils, as shown by CD11b-dependent CD69 up-regulation on eosinophils [44]. In its function as complement receptor 3, CD11b can support eosinophil degranulation [45].…”

Section: Discussionmentioning

confidence: 99%

Up-regulation of CCL11 and CCL26 is associated with activated eosinophils in bullous pemphigoid

Günther

Wozel

Meurer

et al. 2011

Clinical and Experimental Immunology

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SummaryEosinophils contribute to the pathogenesis of bullous pemphigoid (BP) by secretion of proinflammatory cytokines and proteases. Trafficking of eosinophils into tissue in animal models and asthma depends on interleukin-5 and a family of chemokines named eotaxins, comprising CCL11, CCL24 and CCL26. Up-regulation of CCL11 has been described in BP, but the expression of the other two members of the eotaxin-family, CCL24 and CCL26, has not been investigated. In addition to these chemokines, expression of adhesion molecules associated with eosinophil migration to the skin should be analysed. We demonstrate that similar to CCL11, the concentration of CCL26 was up-regulated in serum and blister fluid of BP patients. In contrast, the concentration of CCL24 was not elevated in sera and blister fluid of the same BP patients. In lesional skin, CCL11 and CCL26 were detected in epidermis and dermis by immunohistochemistry. In contrast to CCL11, CCL26 was expressed strongly by endothelial cells. In line with these findings, eosinophils represented the dominating cell population in BP lesional skin outnumbering other leucocytes. The percentage of eosinophils expressing very late antigen (VLA): VLA-4 (CD49d) and CD11c correlated with their quantity in tissue. Macrophage antigen (MAC)-1 (CD11b/CD18) was expressed constitutively by tissue eosinophils. In conclusion, these data link the up-regulation of the eosinophil chemotactic factor CCL26 in BP to the lesional accumulation of activated eosinophils in the skin. Thereby they broaden the understanding of BP pathogenesis and might indicate new options for therapeutic intervention.

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“…The first is the direct induction of apoptosis of CD4 + T cells and eosinophils in airways. Previous studies revealed that those activated T cells or eosinophils expressing high levels of CD69 are susceptible to spontaneous apoptosis in vitro (Matsumoto et al, 1998;Luttmann et al, 1999;Dallaire et al, 2003;Esplugues et al, 2003;Lewkowich et al, 2005;Wang et al, 2006). This pro-apoptotic effect of CD69 might be explained by the observation that CD69 is associated with the N-terminal fragment of calreticulin, a known apoptosis-inducing signal molecule (Vance et al, 2005).…”

Section: Fig 6 Effect Of Anti-cd69 Mab On Ova-induced Ahrmentioning

confidence: 99%

Anti-CD69 monoclonal antibody treatment inhibits airway inflammation in a mouse model of asthma

Wang

Dai

Wang

et al. 2015

J. Zhejiang Univ. Sci. B

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Abstract:Objective: Airway inflammation and airway hyper-responsiveness (AHR) are principle pathological manifestations of asthma. Cluster of differentiation 69 (CD69) is a well-known co-stimulatory factor associated with the activation, proliferation as well as apoptosis of immune cells. This study aims to examine the effect of anti-CD69 monoclonal antibody (mAb) on the pathophysiology of a mouse model of asthma. Methods: A murine model of ovalbumin (OVA)-induced allergic airway inflammation was used in this study. Briefly, mice were injected with 20 μg chicken OVA intraperitoneally on Days 0 and 14, followed by aerosol provocation with 1% (0.01 g/ml) OVA on Days 24, 25, and 26. Anti-CD69 mAb or isotype IgG was injected intraperitoneally after OVA challenge; dexamethasone (DXM) was administrated either before or after OVA challenge. AHR, mucus production, and eosinophil infiltration in the peribronchial area were examined. The levels of granulocyte-macrophage colony-stimulating factor (GM-CSF) and interleukin-5 (IL-5) in bronchoalveolar lavage fluid (BALF) were also assayed as indices of airway inflammation on Day 28 following OVA injection. Results: Pretreatment with DXM together with anti-CD69 mAb treatment after OVA provocation completely inhibited AHR, eosinophil infiltration and mucus overproduction, and significantly reduced BALF IL-5. However, treatment with DXM alone after OVA challenge only partially inhibited AHR, eosinophil infiltration and mucus overproduction, and did not diminish BALF IL-5. Treatment with either DXM or anti-CD69 mAb did not alter the concentration of BALF GM-CSF. Conclusions: Anti-CD69 mAb treatment inhibits established airway inflammation as effectively as DXM pretreatment. This study provides a potential alternative therapeutic opportunity for the clinical management of asthma and its exacerbation.

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Endothelial cells modulate eosinophil surface markers and mediator release

Cited by 42 publications

References 46 publications

Vascular cell adhesion molecule 1 (VCAM-1) activation of endothelial cell matrix metalloproteinases: role of reactive oxygen species

Vascular cell adhesion molecule 1 (VCAM-1) activation of endothelial cell matrix metalloproteinases: role of reactive oxygen species

Up-regulation of CCL11 and CCL26 is associated with activated eosinophils in bullous pemphigoid

Anti-CD69 monoclonal antibody treatment inhibits airway inflammation in a mouse model of asthma

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