IL-8 and airway neutrophilia in children with gastroesophageal reflux and asthma-like symptoms.

Gastroesophageal reflux (GER) may induce respiratory symptoms (RS) through inhalation of acid gastric contents. To characterize the airway inflammation associated with this condition, 20 children [7.4 (0.

Concentration-dependent activity of mometasone furoate and dexamethasone on blood eosinophils isolated from atopic children: modulation of Mac-1 expression and chemotaxis.

Treatment of asthma with corticosteroids results in downregulation of eosinophilic airway inflammation. We evaluated in vitro the activity of an "inhaled" corticosteroid, mometasone furoate (MF), and of a "systemic" corticosteroid, dexamethasone (DEX), on eosinophil functions, i.e.

Epithelial cells and fibroblasts: structural repair and remodelling in the airways.

Extensive lesions and changes in the architecture of the airway walls are commonly described in patients with respiratory infections, asthma, chronic bronchitis and interstitial lung diseases. Current knowledge identifies in airway epithelial cells and in fibroblasts the two cell types mainly involved in tissue repair after injury. During inflammatory respiratory disorders, extensive injury of airway epithelium may occur, with shedding of a large sheet of damaged cells in the bronchial and alveolar lumen but also with activation of the surviving epithelial cells and of the underlying fibroblasts.

Total and allergen-specific IgE levels in serum reflect blood eosinophilia and fractional exhaled nitric oxide concentrations but not pulmonary functions in allergic asthmatic children sensitized to house dust mites.

Although elevated levels of serum immunoglobulin E (IgE) are considered the hallmark of atopic diseases, their clinical value in evaluating subjects with allergic disorders is under debate. To evaluate possible relationships between serum IgE levels and a variety of clinical parameters, 83 mild asthmatic children [10.98-year-old (2.

Modulation of the constitutive or cytokine-induced bronchial epithelial cell functions in vitro by fluticasone propionate.

When exposed to proinflammatory mediators, human bronchial epithelial cells (HBECs) upregulate the 'constitutive' adhesion molecule expression and cytokine/chemokine release. We tested whether and to what extent the inhibitory effect of fluticasone propionate on HBECs could involve the 'constitutive' and 'cytokine-induced' proinflammatory functions. Stimulation of the HBECs with interleukin (IL)-4 plus tumour necrosis factor (TNF)-alpha was more effective in upregulating intercellular adhesion molecule (ICAM)-1 ( approximately 2.

Correlations between exhaled nitric oxide levels, blood eosinophilia, and airway obstruction reversibility in childhood asthma are detectable only in atopic individuals.

The aim of this study was to compare in atopic and nonatopic asthmatic children correlations between two inflammation parameters, i.e., blood eosinophilia and exhaled nitric oxide (FE(NO)), and pulmonary function values, at baseline and after beta(2)-adrenergic bronchodilators.

Fibroblast-eosinophil interaction: modulation of adhesion molecules expression and chemokine release by human fetal lung fibroblasts in response to IL-4 and TNF-alpha.

In addition to be involved in airway remodelling observed in asthmatic patients, lung fibroblasts may directly contribute to pulmonary inflammation through the release of mediators and through the expression of surface molecules involved in cell-cell interaction. The aim of the study was to evaluate whether two cytokines involved in asthma pathogenesis, IL-4 and TNF-alpha, could modulate the expression of adhesion molecules (VCAM-1 and ICAM-1) and the secretion of chemokines (eotaxin and MCP-1) related to eosinophil recruitment and activation. The constitutive expression of VCAM-1 by unstimulated fibroblasts was over 2-fold lower than that of ICAM-1 (P<0.