Effect of hydrogen sulfide (H2S) on airways remodeling, eosinophil apoptosis and cytokines levels in allergic pulmonary inflammation in mice

• Grant number: 12/02145-3
• Support Opportunities: Regular Research Grants
• Start date: July 01, 2012
• End date: June 30, 2014
• Field of knowledge: Biological Sciences - Pharmacology
• Principal Investigator: Heloisa Helena de Araujo Ferreira
• Grantee: Heloisa Helena de Araujo Ferreira
• Host Institution: Universidade São Francisco (USF). Campus Bragança Paulista. Bragança Paulista , SP, Brazil
• City of the host institution: Bragança Paulista

Abstract

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 to verify if the beneficial effect of H2S on pulmonary allergic inflammation in lung tissue is a consequence of its eosinophil pro-apoptotic effect as well as its role on airways remodeling. It will also be observed the H2S action on the levels of cytokines related to allergy and/or cell apoptosis, such as IL-1beta, IL-4, IL-5, IL-10, IL-25, TNF-alfa, eotaxin, TGF-beta1 and VEGF. (AU)

Scientific publications

(The scientific publications listed on this page originate from the Web of Science or SciELO databases. Their authors have cited FAPESP grant or fellowship project numbers awarded to Principal Investigators or Fellowship Recipients, whether or not they are among the authors. This information is collected automatically and retrieved directly from those bibliometric databases.)

CAMPOS, DAIANA; RAVAGNANI, FELIPE G.; GURGUEIRA, SONIA A.; VERCESI, ANIBAL E.; TEIXEIRA, SIMONE A.; COSTA, SORAIA K. P.; MUSCARA, MARCELO N.; FERREIRA, HELOISA H. A.. Increased glutathione levels contribute to the beneficial effects of hydrogen sulfide and inducible nitric oxide inhibition in allergic lung inflammation. International Immunopharmacology, v. 39, p. 57-62, OCT 2016. (14/24518-1, 12/02145-3, 13/04151-3)