Interaction of Human Mast Cell Tryptase with Endothelial Cells to Stimulate Inflammatory Cell Recruitment

1999 ◽  
Vol 118 (2-4) ◽  
pp. 204-205 ◽  
Author(s):  
Steven J. Compton ◽  
Jennifer A. Cairns ◽  
Stephen T. Holgate ◽  
Andrew F. Walls
Keyword(s):  
Endothelial Cells ◽  
Mast Cell ◽  
Inflammatory Cell ◽  
Human Mast Cell ◽  
Mast Cell Tryptase ◽  
Cell Recruitment ◽  
Inflammatory Cell Recruitment

scholarly journals The Role of PPARs in the Endothelium: Implications for Cancer Therapy

PPAR Research ◽  
2008 ◽  
Vol 2008 ◽  
pp. 1-12 ◽  
Author(s):  
David Bishop-Bailey ◽  
Karen E. Swales
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Platelet Activation ◽  
Inflammatory Cell ◽  
Cell Layer ◽  
Cell Recruitment ◽  
Blood Vessel Formation ◽  
Endothelial Cell Layer ◽  
Inflammatory Cell Recruitment

The growth and metastasis of cancers intimately involve the vasculature and in particular the endothelial cell layer. Tumours require new blood vessel formation via angiogenesis to support growth. In addition, inflammation, coagulation, and platelet activation are common signals in the growth and metastasis of tumour cells. The endothelium plays a central role in the homeostatic control of inflammatory cell recruitment, regulating platelet activation and coagulation pathways. PPAR, -/, and - are all expressed in endothelial cells. This review will discuss the roles of PPARs in endothelial cells in relation to angiogenesis, inflammation, coagulation, and platelet control pathways. In particular, we will discuss the recent evidence that supports the hypothesis that PPAR and PPAR are antiangiogenic receptors, while PPAR/ is proangiogenic.

scholarly journals TRAF5 Deficiency Accelerates Atherogenesis in Mice by Increasing Inflammatory Cell Recruitment and Foam Cell Formation

2010 ◽  
Vol 107 (6) ◽  
pp. 757-766 ◽  
Author(s):  
Anna Missiou ◽  
Philipp Rudolf ◽  
Peter Stachon ◽  
Dennis Wolf ◽  
Nerea Varo ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Inflammatory Cell ◽  
Foam Cell ◽  
Interleukin 1 ◽  
Cell Formation ◽  
Foam Cell Formation ◽  
High Cholesterol Diet ◽  
Cell Recruitment ◽  
Inflammatory Cell Recruitment

Rationale: Tumor necrosis factor receptor–associated factors (TRAFs) are cytoplasmic adaptor proteins for the TNF/interleukin-1/Toll-like receptor superfamily. Ligands of this family comprise multiple important cytokines such as TNFα, CD40L, and interleukin-1β that promote chronic inflammatory diseases such as atherosclerosis. We recently reported overexpression of TRAF5 in murine and human atheromata and that TRAF5 promotes inflammatory functions of cultured endothelial cells and macrophages. Objective: This study tested the hypothesis that TRAF5 modulates atherogenesis in vivo. Methods and Results: Surprisingly, TRAF5 −/− /LDLR −/− mice consuming a high-cholesterol diet for 18 weeks developed significantly larger atherosclerotic lesions than did TRAF5 +/+ /LDLR −/− controls. Plaques of TRAF5-deficient animals contained more lipids and macrophages, whereas smooth muscle cells and collagen remained unchanged. Deficiency of TRAF5 in endothelial cells or in leukocytes enhanced adhesion of inflammatory cells to the endothelium in dynamic adhesion assays in vitro and in murine vessels imaged by intravital microscopy in vivo. TRAF5 deficiency also increased expression of adhesion molecules and chemokines and potentiated macrophage lipid uptake and foam cell formation. These findings coincided with increased activation of JNK and appeared to be independent of TRAF2. Finally, patients with stable or acute coronary heart disease had significantly lower amounts of TRAF5 mRNA in blood compared with healthy controls. Conclusions: Unexpectedly, TRAF5 deficiency accelerates atherogenesis in mice, an effect likely mediated by increased inflammatory cell recruitment to the vessel wall and enhanced foam cell formation.

scholarly journals Expression and Function of the Homeostatic Molecule Del-1 in Endothelial Cells and the Periodontal Tissue

2013 ◽  
Vol 2013 ◽  
pp. 1-12 ◽  
Author(s):  
Jieun Shin ◽  
Kavita B. Hosur ◽  
Kalyani Pyaram ◽  
Ravi Jotwani ◽  
Shuang Liang ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Adhesion Molecule ◽  
Inflammatory Cell ◽  
Leukocyte Adhesion ◽  
Neutrophil Infiltration ◽  
Intercellular Adhesion Molecule ◽  
Adhesion Molecule Expression ◽  
Reciprocal Regulation ◽  
Cell Recruitment ◽  
Inflammatory Cell Recruitment

Developmental endothelial locus-1 (Del-1) is an endothelial cell-secreted protein that limits the recruitment of neutrophils by antagonizing the interaction between the LFA-1 integrin on neutrophils and the intercellular adhesion molecule (ICAM)-1 on endothelial cells. Mice with genetic or age-associated Del-1 deficiency exhibit increased neutrophil infiltration in the periodontium resulting in inflammatory bone loss. Here we investigated additional novel mechanisms whereby Del-1 could interfere with neutrophil recruitment and inflammation. Treatment of human endothelial cells with Del-1 did not affect the expression of endothelial molecules involved in the leukocyte adhesion cascade (ICAM-1, VCAM-1, and E-selectin). Moreover, genetic or age-associated Del-1 deficiency did not significantly alter the expression of these adhesion molecules in the murine periodontium, further ruling out altered adhesion molecule expression as a mechanism whereby Del-1 regulates leukocyte recruitment. Strikingly, Del-1 inhibited ICAM-1-dependent chemokine release (CXCL2, CCL3) by neutrophils. Therefore, Del-1 could potentially suppress the amplification of inflammatory cell recruitment mediated through chemokine release by infiltrating neutrophils. Interestingly, Del-1 was itself regulated by inflammatory stimuli, which generally exerted opposite effects on adhesion molecule expression. The reciprocal regulation between Del-1 and inflammation may contribute to optimally balance the protective and the potentially harmful effects of inflammatory cell recruitment.

scholarly journals Lung endothelial cell platelet-activating factor production and inflammatory cell adherence are increased in response to cigarette smoke component exposure

2012 ◽  
Vol 302 (1) ◽  
pp. L47-L55 ◽  
Author(s):  
Janhavi Sharma ◽  
Dawn M. Young ◽  
John O. Marentette ◽  
Prerna Rastogi ◽  
John Turk ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Cigarette Smoke ◽  
Inflammatory Cell ◽  
Platelet Activating Factor ◽  
Small Airways ◽  
Cell Adherence ◽  
Cell Recruitment ◽  
Raw 264.7 Cell ◽  
Inflammatory Cell Recruitment ◽  
Lung Endothelial Cells

An early event in the pathogenesis of emphysema is the development of inflammation associated with accumulation of polymorphonuclear leukocytes (PMN) in small airways, and inflammatory cell recruitment from the circulation involves migration across endothelial and epithelial cell barriers. Platelet-activating factor (PAF) promotes transendothelial migration in several vascular beds, and we postulated that increased PAF production in the airways of smokers might enhance inflammatory cell recruitment and exacerbate inflammation. To examine this possibility, we incubated human lung microvascular endothelial cells (HMVEC-L) with cigarette smoke extract (CSE) and found that CSE inhibits PAF-acetylhydrolase (PAF-AH) activity. This enhances HMVEC-L PAF production and PMN adherence, and adherence is blocked by PAF receptor antagonists (CV3988 or ginkgolide B). CSE also inhibited PAF-AH activity of lung endothelial cells isolated from wild-type (WT) and iPLA2β knockout mice, and with WT cells, CSE enhanced PAF production and RAW 264.7 cell adherence. In contrast, CSE did not affect PAF production or RAW 264.7 cell adherence to iPLA2β-null cells, suggesting that iPLA2β plays an important role in PAF production by lung endothelial cells. These findings suggest that inhibition of PAF-AH by components of cigarette smoke may initiate or exacerbate inflammatory lung disease by enhancing PAF production and promoting accumulation of inflammatory cells in small airways. In addition, iPLA2β is identified as a potential target for therapeutic interventions to reduce airway inflammation and the progression of chronic lung disease.

scholarly journals Chemokine Receptor Ccr6 Deficiency Alters Hepatic Inflammatory Cell Recruitment and Promotes Liver Inflammation and Fibrosis

PLoS ONE ◽  
2015 ◽  
Vol 10 (12) ◽  
pp. e0145147 ◽  
Author(s):  
Silvia Affò ◽  
Daniel Rodrigo-Torres ◽  
Delia Blaya ◽  
Oriol Morales-Ibanez ◽  
Mar Coll ◽  
...  
Keyword(s):  
Chemokine Receptor ◽  
Inflammatory Cell ◽  
Liver Inflammation ◽  
Cell Recruitment ◽  
Inflammatory Cell Recruitment

scholarly journals The Flavonoid Isoliquiritigenin Reduces Lung Inflammation and Mouse Morbidity during Influenza Virus Infection

2015 ◽  
Vol 59 (10) ◽  
pp. 6317-6327 ◽  
Author(s):  
Hussein Traboulsi ◽  
Alexandre Cloutier ◽  
Kumaraswamy Boyapelly ◽  
Marc-André Bonin ◽  
Éric Marsault ◽  
...  
Keyword(s):  
Influenza Virus ◽  
Virus Infection ◽  
Inflammatory Response ◽  
Lung Inflammation ◽  
Inflammatory Cell ◽  
Influenza Virus Infection ◽  
Cytokine Gene Expression ◽  
Cell Recruitment ◽  
Inflammatory Cell Recruitment ◽  
Anti Inflammatory

ABSTRACTThe host response to influenza virus infection is characterized by an acute lung inflammatory response in which intense inflammatory cell recruitment, hypercytokinemia, and a high level of oxidative stress are present. The sum of these events contributes to the virus-induced lung damage that leads to high a level of morbidity and mortality in susceptible infected patients. In this context, we identified compounds that can simultaneously reduce the excessive inflammatory response and the viral replication as a strategy to treat influenza virus infection. We investigated the anti-inflammatory and antiviral potential activities of isoliquiritigenin (ILG). Interestingly, we demonstrated that ILG is a potent inhibitor of influenza virus replication in human bronchial epithelial cells (50% effective concentration [EC50] = 24.7 μM). In addition, our results showed that this molecule inhibits the expression of inflammatory cytokines induced after the infection of cells with influenza virus. We demonstrated that the anti-inflammatory activity of ILG in the context of influenza virus infection is dependent on the activation of the peroxisome proliferator-activated receptor gamma pathway. Interestingly, ILG phosphate (ILG-p)-treated mice displayed decreased lung inflammation as depicted by reduced cytokine gene expression and inflammatory cell recruitment. We also demonstrated that influenza virus-specific CD8+effector T cell recruitment was reduced up to 60% in the lungs of mice treated with ILG-p (10 mg/kg) compared to that in saline-treated mice. Finally, we showed that administration of ILG-p reduced lung viral titers and morbidity of mice infected with the PR8/H1N1 virus.

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