Source and nature of inhaled atmospheric dust from trace element analyses of human bronchial fluids.

Rapid volcanic eruptions quickly ejecting large amounts of dust provoke the accumulation of heavy metals in people living in surrounding areas. Analyses of bronchoalveolar lavage samples (BAL) collected from people exposed to the paroxysmal 2001 Etna eruption revealed a strong enrichment of many toxic heavy metals. Comparing the BAL to the dust composition of southeastern Sicily, we found that only V, Cr, Mn, Fe, Co, and U enrichment could be related to the volcanic event, whereas Ni, Cu, Cd, and Pb contents come from the dissolution of particles of anthropogenic origin.

Anti-inflammatory effects of pre-seasonal Th1-adjuvant vaccine to Parietaria judaica in asthmatics.

Background: The ultra-short course pre-seasonal allergy vaccine, containing appropriate allergoids with the adjuvant monophosphoryl lipid A (MPL), may be effective in treating allergic symptoms.

Objective: To explore the timing of the immunological responses to the pre-seasonal allergy vaccine.

Methods: Four subcutaneous injections of the active product (Pollinex Quattro) were administered to 20 Parietaria-sensitive intermittent asthmatics (M/F: 12/8; age: 48 ± 10 years; FEV(1)% predicted: 108% ± 12%) during the 6 weeks prior to the start of the pollen season.

The effect of intranasal corticosteroids on asthma control and quality of life in allergic rhinitis with mild asthma.

Background: The mechanisms through which rhinitis affects asthma have not been completely elucidated. We explored whether the effect of nasal treatment on asthma control and respiratory-related quality of life (HRQoL) is mediated by inflammatory changes of the upper and lower airways.

Methods: Allergic rhinitics with mild asthma were randomized to a 14-day treatment period with either nasal budesonide 100 μg, 1 puff per nostril twice a day, or placebo.

Altered CD94/NKG2A and perforin expression reduce the cytotoxic activity in malignant pleural effusions.

CD94/NKG2A is an inhibitory receptor expressed by NK cells and cytotoxic lymphocytes and, upon activation by HLA-E, downregulates the cytolytic activities of these cells thus representing a tumour immune escape mechanism. This study was aimed at assessing whether cytotoxic lymphocytes (CD8+) and NK cells from malignant pleural effusions have a deregulated expression of CD94/NKG2A. The expression of membrane CD94/NKG2A and perforin was evaluated by flow-cytometry in CD8+ and NK cells from pleural effusions and autologous peripheral blood of cancer (n=19) and congestive heart failure (CHF) (n=11) patients.

Effects of exercise training on airway responsiveness and airway cells in healthy subjects.

Airway responsiveness to methacholine (Mch) in the absence of deep inspirations (DIs) is lower in athletes compared with sedentary individuals. In this prospective study, we tested the hypothesis that a training exercise program reduces the bronchoconstrictive effect of Mch. Ten healthy sedentary subjects (M/F: 3/7; mean + or - SD age: 22 + or - 3 yr) entered a 10-wk indoor rowing exercise program on rowing ergometer and underwent Mch bronchoprovocation in the absence of DIs at baseline, at weeks 5 and 10, as well as 4-6 wk after the training program was completed.

Bronchial epithelial damage after a half-marathon in nonasthmatic amateur runners.

High neutrophil counts in induced sputum have been found in nonasthmatic amateur runners at rest and after a marathon, but the pathogenesis of airway neutrophilia in athletes is still poorly understood. Bronchial epithelial damage may occur during intense exercise, as suggested by investigations conducted in endurance-trained mice and competitive human athletes studied under resting conditions. To gain further information on airway changes acutely induced by exercise, airway cell composition, apoptosis, IL-8 concentration in induced sputum, and serum CC-16 level were measured in 15 male amateur runners at rest (baseline) and shortly after a half-marathon.

CD40 ligation protects bronchial epithelium against oxidant-induced caspase-independent cell death.

CD40 and its ligand regulate pleiotropic biological responses, including cell proliferation, differentiation, and apoptosis. In many inflammatory lung diseases, tissue damage by environmental or endogenous oxidants plays a major role in disease pathogenesis. As the epithelial barrier is a major target for these oxidants, we postulated that CD40, the expression of which is increased in asthma, plays a role in the regulation of apoptosis of bronchial epithelial cells exposed to oxidants.