Soluble human leucocyte antigen-G and interleukin-10 levels in isocyanate-induced asthma.

BACKGROUND: We previously reported that in moderate-to-severe asthma there is a deficit of IL-10 secretion that could prevent the production of soluble HLA-G (sHLA-G), a non-classical human leucocyte antigen class I molecule with tissue-protective properties in inflammatory responses. OBJECTIVE: Our objective was to investigate the production of sHLA-G and the secretion of IL-10 by peripheral blood mononuclear cells (PBMCs) in asthma induced by isocyanates and to compare the results with those obtained in non-occupational allergic asthma. METHOD: sHLA-G and IL-10 were measured by ELISA in the culture supernatants of unstimulated or lipopolysaccharide (LPS)-stimulated PBMCs obtained from 20 subjects with isocyanate asthma, 16 asymptomatic subjects exposed to isocyanates, 18 subjects with non-occupational allergic asthma, and 26 healthy control subjects. RESULTS: Occupational exposure to isocyanates was associated with high baseline levels of secretion of IL-10 by PBMCs, whether or not the exposed subjects had asthmatic symptoms. However, spontaneous production of sHLA-G by PBMC was significantly higher in subjects with isocyanate asthma compared with asymptomatic-exposed controls. In contrast, PBMCs from subjects with non-occupational allergic asthma produced sHLA-G only after LPS stimulation. CONCLUSIONS: sHLA-G production and IL-10 secretion are influenced by workplace exposure to isocyanates and by development of asthma. The different behaviour of both sHLA-G and IL-10 in asthma induced by isocyanates compared with non-occupational allergic asthma suggests a heterogeneous biological role for HLA-G molecules and for IL-10, a key cytokine of immune and inflammatory responses.

[Acute effects of environmental pollution on the urban vigilants airways]. / Effetto acuto dell'inquinamento ambientale sulle vie aeree in vigili urbani.

AIM OF THE STUDY: The purpose of this study was to evaluate whether the acute exposure to air pollution, in a group of policemen of Padua, is correlated with increased inflammatory biomarkers (exhaled nitric oxide, feNO) and alterations of bronchiolar cells (assessed by CC16 Clara cell-specific protein). METHODS: We studied 44 healthy, non-smokers divided in exposed to traffic and controls (office workers). Before and after the Monday shift serum and urinary concentration of CC16, feNo and spirometry were measured in each subject. Data on air pollutants, PM2.5, PM10, SO2, NO2, CO, O3 were collected from official bulletin online (ARPAV). RESULTS: In exposed policemen serum CC16 decreased after shift (before 4.6 +/- 0.2 vs after 6.4 +/- 0.8 ng/ml, = 0.02), while feNO increased significantly (33.2 +/- 4.4 vs 29.7 +/- 3.9 ppb, p = 0.02). feNO cross-shift changes were positively correlated with environmental SO2 levels (rho = 0.48; p = 0.01). CONCLUSIONS: Our results suggest that in healthy and nonsmokers subjects the exposure to air pollution is associated with subclinical airway inflammation and decrease of bronchiolar epithelium function.