Urokinase Localization and Activity in Isolated Eosinophils

Mabilat-Pragnon, C; Janin, Anne; Michel, Laurence; Thomaidis, Annick; Legrand, Yves; Soria, Claudine; Lű, He

doi:10.1016/s0049-3848(97)00268-5

Cited by 14 publications

(10 citation statements)

References 16 publications

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“…7, can be associated with the increased pulmonary eosinophilia, macrophage activation, and airway damage observed in ADA-deficient lungs. Several molecules such as uPA and its receptor (CD87), along with B7.2, are genes known to regulate the development of murine allergic asthma by mediating inflammatory cell influx (26,29). In addition, the role of adhesion molecules intercellular adhesion molecule-1, P-selectin, and leukocyte adhesion protein-1 in mediating eosinophil trafficking in a murine model of pulmonary inflammation is well documented (7,8).…”

Section: Discussionmentioning

confidence: 99%

Gene expression profiling in inflammatory airway disease associated with elevated adenosine

Banerjee

Young

Volmer

et al. 2002

American Journal of Physiology-Lung Cellular and Molecular Phys

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Adenosine has been implicated as a modulator of inflammatory processes central to asthma. However, the molecular mechanisms involved are poorly understood. We used Atlas mouse cDNA arrays to analyze differential gene expression in association with lung inflammation resulting from elevated adenosine in adenosine deaminase (ADA)-deficient mice. We report that of the 1,176 genes on the array, the expression patterns of 280 genes were consistently altered. Of these genes, the steady-state levels of 93 genes were upregulated and 29 were downregulated. We also show that lowering adenosine levels with ADA enzyme therapy has striking effects on gene expression that may be associated with resolution of pulmonary eosinophilia. In addition, we confirmed the nucleic acid and protein expression of vascular endothelial growth factor and monocyte chemoattractant protein-3, two candidate genes that may be regulated by adenosine. In conclusion, high-throughput profiling of gene expression by cDNA array hybridization has provided an overview of critical regulatory genes involved in airway inflammation in ADA-deficient mice. These mice will serve as a useful in vivo model for characterizing molecular mechanisms of adenosine-mediated lung damage.

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Section: Discussionmentioning

confidence: 99%

Gene expression profiling in inflammatory airway disease associated with elevated adenosine

Banerjee

Young

Volmer

et al. 2002

American Journal of Physiology-Lung Cellular and Molecular Phys

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“…In the late fibrotic stage with endomyocardial fibrosis, cardiac damage involves atrioventricular valves and induces congestive heart failure. Independently of endomyocardial lesions, peripheral thromboembolism related to an increased number of blood eosinophils may occur (Mabilat‐Pragnon et al , 1997; Alter and Maisch, 2006).…”

Section: Diagnostic Criteria For Hesmentioning

confidence: 99%

Oral mucosa lesions in hypereosinophilic syndrome – an update

2008

Self Cite

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Hypereosinophilic syndrome (HES) is a rare disorder characterized by persistent and marked eosinophilia. Some HES forms have a poor prognosis, either because of end-organ damage (particularly endomyocardial fibrosis), or because of associated myeloid leukemia or malignant T-cell lymphoma. Oral mucosa ulcerations can be early clinical signs in severe forms. They are discrete, round or oval, sometimes confluent ulcers or erosions, located on non-keratinized, unattached oral mucosa. In the last 15 years a better understanding of eosinophil biology has led to a new clinical classification of HES. The lymphocytic form is characterized by T-lymphocyte clonality, IL-5 production, and a possible progression to T-cell lymphoma. Oral lesions are more frequently associated with the myeloproliferative form, characterized by an increased risk of developing myeloid malignancies and a good response to a recent anti-tyrosine kinase therapy (imatinib mesylate). The target of imatinib is a novel kinase resulting from an 800-kb deletion on chromosome 4. Recently, the resulting FIP1L1-PDGFRalpha fusion gene was characterized as a marker of response to imatinib. Exclusion of other erosive ulcerative oral disease and early recognition of HES in patients with oral ulcerations, and precise characterization of the lymphocytic or myeloproliferative form are therefore important to rapidly initiate an effective therapy.

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“…Components of the system are expressed by numerous different cell types, and they are important regulators and mediators of immune inflammatory processes, partly because of their participation in mechanisms mediating recruitment and migration of cells as well as inflammatory mediators and immune stimuli affecting their synthesis [1,2]. The cells playing the key role in allergic inflammation are also capable of expressing functionally either active uPA or its receptor or both, including dendritic cells [3], eosinophils [4,5], and mast cells [6]. In addition, uPAR expression on eosinophils from normal and asthmatic patients was increased by IL-5 [5].…”

Section: Introductionmentioning

confidence: 99%

The urokinase system in patients with intermittent and persistent allergic rhinitis

Kasperska−Zając

Brzoza²,

Rogala³

2008

Blood Coagulation &Amp; Fibrinolysis

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Local and systemic changes in hemostasis are associated with allergic diseases. Apart from their well documented role in regulation of plasminogen activation, components of the urokinase system may be involved in modulation of cellular activities during immune inflammatory responses. So far, little has been known about the function of the system in allergic inflammation. In the present study, we assessed circulating levels of the urokinase system components such as urokinase-type plasminogen activator (uPA), soluble form of uPA receptor (CD87), and the inhibitor--plasminogen activator inhibitor type 1. The study comprised of patients suffering from allergic rhinitis, however, without any asthmatic symptoms. Plasma levels of uPA and soluble form of uPA receptor antigens, and plasminogen activator inhibitor type 1 activity were measured in 17 patients with grass pollens-induced intermittent allergic rhinitis and 15 patients with persistent allergic rhinitis due to house dust mite allergy, as well as in 20 sex-matched and age-matched healthy nonatopic participants. We did not observe any statistically significant differences in the levels of the urokinase system components between patients with intermittent allergic rhinitis and persistent allergic rhinitis, and the controls. The circulating levels of uPA, its soluble receptor, and its inhibitor did not differ between allergic rhinitis patients and healthy participants, therefore it seems that the systemic release and activity of the urokinase system molecules may be not significantly changed in the course of nasal allergic inflammation induced by periodic or continuous exposure to a natural allergen.

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Urokinase Localization and Activity in Isolated Eosinophils

Cited by 14 publications

References 16 publications

Gene expression profiling in inflammatory airway disease associated with elevated adenosine

Gene expression profiling in inflammatory airway disease associated with elevated adenosine

Oral mucosa lesions in hypereosinophilic syndrome – an update

The urokinase system in patients with intermittent and persistent allergic rhinitis

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