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• W67463089 abstract "ABSTRACTBackground: The bleomycin is a glycopeptide with antitumor and antiviral activity utilized in clinical for chemotherapeutic treatment of several neoplasms. Unfortunately the 10% of treated patients develops interstitial pneumonia that progresses to fibrosis. The fibrogenesis is linked to develop of a Th2 cellular response with proinflammatory chemokines release.Glycogen Synthase Kinase 3 (GSK-3) is a pivotal element for the control of immune response because modulates the inflammatory cytokines production. Since lung injury caused by bleomycin is characterized by an inflammatory response followed by a fibrotic degeneration, we postulated that blocking GSK-3 kinase activity with a specific inhibitor could affect the bleomycin-induced pulmonary inflammatory and pro-fibrotic cytokine network. Moreover it has been demonstrated that the develop of pathologies which elicit a Th2 inflammatory response could be mitigated by agents able to induce a Th1 immune response. Indeed administration of Neutrophil-Activating Protein of Helicobacter pylori (HP-NAP) was found to be able to down modulate the Th2 immune response in a asthma ovalbumin-induced model mouse by eliciting a Th1 immune response and resulted effective in preventing allergic asthma in the model mouse.Purpose of the study: We investigated the effects of the specific and selective ATP-competitive GSK-3 inhibitor, SB216763, and the effects of HP-NAP administration on the onset and development of inflammation and fibrosis in a bleomycin-induced lung fibrosis mouse model. Methods: We differently randomised cohorts of C57BL6 mice to receive intratracheal instillation of inhibitor SB216763, HP-NAP, bleomycin, bleomycin plus SB216763 or bleomycin plus HP-NAP and followed their health status for 28 days. Bronchoalveolar lavage (BAL) was performed and mice were sacrificed at different interval times (2, 7, 14 and 28 days). Histopathological analysis of the lungs, flow-cytometry studies and Cell Sorting of BAL pulmonary monocytes were then performed. Finally we examined cytokines gene expression levels in lung monocytes trough Real Time PCR analysis. Results: SB216763 and HP-NAP administration prevented lung inflammation and the subsequent fibrosis when co-administrated with bleomycin. BALF analysis of mice revealed a significant reduction in bleomycin-induced alveolitis. SB216763 treatment was associated with a significantly lower production of inflammatory cytokines (TNF-α and CCL12) by macrophages. Moreover we observed that HP-NAP administration downmodulated the Th2 inflammatory response bleomycin-induced by eliciting a Th1 phenotype (downmodulating IL-4 chemokine and upregulating the IFN-γ).Conclusions: These findings suggest that GSK-3 inhibition induces a protective effect on lung fibrosis triggered by bleomycin and candidate GSK-3 as a potential therapeutic target for preventing pulmonary fibrosis. Furthermore our results suggest that also HP-NAP, preventing lung fibrosis develop, might be a possible new tool for therapeutic strategies aimed to redirect Th2 into less aggressive Th1 response." @default.
• W67463089 created "2016-06-24" @default.
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• W67463089 date "2009-03-13" @default.
• W67463089 modified "2023-09-24" @default.
• W67463089 title "Role of inflammation in the development of lung fibrosis and in the pathogenesis of pulmunary hypertension" @default.
• W67463089 hasPublicationYear "2009" @default.
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