Bertolino, Antonio (2015) Role of sphingolipid and hydrogen sulphide pathways in inflammatory lung diseases. [Tesi di dottorato]


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Item Type: Tesi di dottorato
Lingua: English
Title: Role of sphingolipid and hydrogen sulphide pathways in inflammatory lung diseases
Date: 31 March 2015
Number of Pages: 187
Institution: Università degli Studi di Napoli Federico II
Department: Farmacia
Scuola di dottorato: Scienze farmaceutiche
Dottorato: Scienza del farmaco
Ciclo di dottorato: 27
Coordinatore del Corso di dottorato:
D'Auria, Maria
Cirino, GiuseppeUNSPECIFIED
Date: 31 March 2015
Number of Pages: 187
Uncontrolled Keywords: sphingosine 1-phosphate, hydrogen sulphide, asthma, pulmonary hypertension, inflammation, airway hyperreactivity, lung pathophysiology, immunology
Settori scientifico-disciplinari del MIUR: Area 05 - Scienze biologiche > BIO/14 - Farmacologia
Date Deposited: 10 Apr 2015 11:49
Last Modified: 28 Apr 2017 01:00
DOI: 10.6092/UNINA/FEDOA/10531


The importance of sphingolipids in lung pathophysiology is becoming more and more evident over years. Despite the findings that they have such numerous activities on cells, the mechanisms by which sphingolipids elicit their effects are not fully understood. Furthermore, the role of other recently-identified mediators such as gasotransmitters in pulmonary district has started to be investigated. My project aimed at clarifying the cellular/molecular pathways underlying the beneficial/detrimental effects of these mediators in lungs in animal experimental models by means of in vivo and in vitro approaches. The results obtained showed that systemic administration of S1P could induce an asthma-like condition in mice and such condition involved the cooperation and activation of different cells of the immune system, i.e. mast cells and T cells. The effects of S1P were counteracted by B cells. Conversely to the negative effects of S1P, we showed that H2S inhalation proved to be beneficial in reducing allergen-induced airway hyperreactivity via a mast cell- and fibroblast-mediated mechanisms, without affecting lung inflammation. However, in an experimental model of pulmonary hypertension, we observed that H2S acted as an antiinflammatory agent. In conclusion, a new experimental asthma-like model useful for defining the role of S1P in the mechanism of action of currently-used drugs as well as in the development of new therapeutic approaches has been characterised. In addition, the protective properties of H2S have been further clarified, evidencing its involvement in modulating remodeling processes in inflammatory lung diseases.


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