Publications by authors named "Imane Bara"

We compared the proliferation of neonatal and adult airway smooth muscle cells (ASMC) with no/moderate lung disease, in glucose- (energy production by glycolysis) or glucose-free medium (ATP production from mitochondrial oxidative phosphorylations only), in response to 10% fetal calf serum (FCS) and PDGF-AA. In the presence of glucose, cell counts were significantly greater in neonatal vs. adult ASMC.

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Asthmatic bronchial smooth muscle (BSM) is characterized by structural remodeling associated with mast cell infiltration displaying features of chronic degranulation. Mast cell-derived tryptase can activate protease activated receptor type-2 (PAR-2) of BSM cells. The aims of the present study were (i) to evaluate the expression of PAR-2 in both asthmatic and non asthmatic BSM cells and, (ii) to analyze the effect of prolonged stimulation of PAR-2 in asthmatic BSM cells on cell signaling and proliferation.

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Rationale: Bronchial remodeling, including increased bronchial smooth muscle (BSM) mass, contributes to bronchial obstruction in asthma. However, its mechanisms are complex and remain controversial. Recently, a role of the chitinase 3-like 1 protein (YKL-40) has been evoked in asthma.

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Asthma is characterized by the association of airway hyperresponsiveness (AHR), inflammation, and remodelling. The aim of the present article is to review the pivotal role of airway smooth muscle (ASM) in the pathophysiology of asthma. ASM is the main effector of AHR.

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Asthma pathophysiology involves bronchial hyperreactivity, inflammation and remodelling, these features being closely linked. Bronchial hyperreactivity is characterized by an excessive airway response to a wide range of stimuli. Bronchial inflammation is characterized by an infiltration of all layers of the bronchial wall by a variety of inflammatory cells, especially mast cells, lymphocytes and eosinophils.

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The chronic inflammatory response within the airways of asthmatics is associated with structural changes termed airway remodeling. This remodeling process is a key feature of severe asthma. The 5-10% of patients with a severe form of the disease account for the higher morbidity and health costs related to asthma.

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Background: Fractional exhaled nitric oxide (F(E)NO) is a marker of airway inflammation in asthma. Monitoring of such inflammation is currently not included in asthma guidelines and remains controversial. The hypothesis underlying the present study was that, F(E)NO could help assessing asthma control and, therefore, improve its management, by predicting loss of control in asthmatics.

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