Allergic asthma is a disease characterized by bronchial airway hyperactivity and chronic airway inflammation with significant infiltration of eosinophils, mast cells and T helper (Th) lymphocytes. It is recognized that the appearance of allergic inflammation is due to action of cytokines derived from Th1, Th2 and Th3 cells. The Th2 response can be induced by IL-25 that influence the induction and amplification of allergic pulmonary inflammation in rats, possibly by delaying the apoptosis and, consequently, promoting the persistence of eosinophils into the airways of asthmatic patients. Among the gaseous radicals that possess important physiological and pathophysiological function, much attention has been given to hydrogen sulfide (H2S) that showed to be involved in the pathogenesis of inflammation and airway remodeling. H2S could also reduced IL-6 and IL-8 levels in non-allergic inflammation model, besides inhibition of IL-1beta, IL -6, TNF-alfa synthesis and increase of IL-10 in cultured macrophages. Recent research from our laboratory demonstrated that treatment with H2S donor, sodium hydrosulfate - NaHS, produced a beneficial effect on asthma by decreasing eosinophil infiltration and oxidative stress in lungs of allergic mice and by reducing goblet cell hyperplasia and mucus plugging in the airways, suggesting that H2S plays an important anti-inflammatory role in allergic lung inflammation. The objective of the present research is verify the effect of H2S on airways remodeling and on the levels of cytokines related to allergy such as IL-1beta, IL-4, IL-5, IL-10, IL-25, TNF-alfa, eotaxin, TGF-beta1 and VEGF.
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