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IL-17A-associated IKK-α signaling induced TSLP production in epithelial cells of COPDpatients
Giulia Anzalone,Giusy Daniela Albano,Angela Marina Montalbano,Loredana Riccobono,Anna Bonanno,Rosalia Gagliardo,Fabio Bucchieri,Roberto Marchese,Monica Moscato,Mirella Profita 생화학분자생물학회 2018 Experimental and molecular medicine Vol.50 No.-
Thymic stromal lymphopoietin (TSLP) is a cytokine expressed in the epithelium, involved in the pathogenesis of chronic disease. IL-17A regulates airway inflammation, oxidative stress, and reduction of steroid sensitivity in chronic obstructive pulmonary disease (COPD). TSLP and IL-17A were measured in induced sputum supernatants (ISs) from healthy controls (HC), healthy smokers (HS), and COPD patients by enzyme-linked immunosorbent assay. Human bronchial epithelial cell line (16HBE) and normal bronchial epithelial cells were stimulated with rhIL-17A or ISs from COPD patients to evaluate TSLP protein and mRNA expression. The effects of the depletion of IL-17A in ISs, an anticholinergic drug, and the silencing of inhibitor kappa kinase alpha (IKKα) on TSLP production were evaluated in 16HBE cells. Coimmunoprecipitation of acetyl-histone H3(Lys14)/IKKα was evaluated in 16HBE cells treated with rhIL- 17A and in the presence of the drug. TSLP and IL-17A levels were higher in ISs from COPD patients and HS compared with HC. TSLP protein and mRNA increased in 16HBE cells and in normal bronchial epithelial cells stimulated with ISs from COPD patients compared with ISs from HC and untreated cells. IKKα silencing reduced TSLP production in 16HBE cells stimulated with rhIL-17A and ISs from COPD patients. RhIL-17A increased the IKKα/acetyl-histone H3 immunoprecipitation in 16HBE cells. The anticholinergic drug affects TSLP protein and mRNA levels in bronchial epithelial cells treated with rhIL-17A or with ISs from COPD patients, and IKKα mediated acetyl-histone H3(Lys14). IL-17A/IKKα signaling induced the mechanism of chromatin remodeling associated with acetyl-histone H3(Lys14) and TSLP production in bronchial epithelial cells. Anticholinergic drugs might target TSLP derived from epithelial cells during the treatment of COPD.
Performances of JEM-EUSO: angular reconstruction : The JEM-EUSO Collaboration
Adams Jr., J. H.,Ahmad, S.,Albert, J. -N.,Allard, D.,Anchordoqui, L.,Andreev, V.,Anzalone, A.,Arai, Y.,Asano, K.,Ave Pernas, M.,Baragatti, P.,Barrillon, P.,Batsch, T.,Bayer, J.,Bechini, R.,Belenguer, Springer-Verlag 2015 Experimental astronomy Vol.40 No.1
An evaluation of the exposure in nadir observation of the JEM-EUSO mission
Adams, J.H.,Ahmad, S.,Albert, J.N.,Allard, D.,Ambrosio, M.,Anchordoqui, L.,Anzalone, A.,Arai, Y.,Aramo, C.,Asano, K.,Ave, M.,Barrillon, P.,Batsch, T.,Bayer, J.,Belenguer, T.,Bellotti, R.,Berlind, A.A. North-Holland ; Elsevier Science Ltd 2013 Astroparticle physics Vol.44 No.-
We evaluate the exposure during nadir observations with JEM-EUSO, the Extreme Universe Space Observatory, on-board the Japanese Experiment Module of the International Space Station. Designed as a mission to explore the extreme energy Universe from space, JEM-EUSO will monitor the Earth's nighttime atmosphere to record the ultraviolet light from tracks generated by extensive air showers initiated by ultra-high energy cosmic rays. In the present work, we discuss the particularities of space-based observation and we compute the annual exposure in nadir observation. The results are based on studies of the expected trigger aperture and observational duty cycle, as well as, on the investigations of the effects of clouds and different types of background light. We show that the annual exposure is about one order of magnitude higher than those of the presently operating ground-based observatories.