کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
2540364 1559760 2016 6 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Lentivirus expressing soluble ST2 alleviates bleomycin-induced pulmonary fibrosis in mice
موضوعات مرتبط
علوم زیستی و بیوفناوری ایمنی شناسی و میکروب شناسی ایمونولوژی
پیش نمایش صفحه اول مقاله
Lentivirus expressing soluble ST2 alleviates bleomycin-induced pulmonary fibrosis in mice
چکیده انگلیسی


• ST2 improves survival rate and reduces body weight loss in mice induced by bleomycin.
• ST2 attenuates pulmonary inflammatory cell infiltration and fibrotic changes.
• ST2 decreases levels of IL-4, IL-6, IL-13, IL-33, MCP-1, and TGF-β1.
• ST2 increases levels of IFN-γ.
• ST2 may offer a novel therapeutic approach to treat pulmonary fibrotic diseases.

It has been shown that the expression of ST2, a receptor of interleukin (IL)-33, is elevated in the lungs of idiopathic pulmonary fibrosis patients and bleomycin-induced mouse models, however its contribution to the development of pulmonary fibrosis has yet to be tested. In the present study, we treated mice by intranasal instillation of lentivirus expressing soluble ST2 and evaluated lung inflammation and fibrosis in the bleomycin-induced pulmonary fibrosis mouse model. We found that ST2 lentivirus treatment significantly improved survival rate and reduced weight loss compared with controls treated with empty lentivirus. Furthermore, ST2 treatment profoundly attenuated the pulmonary inflammatory cell infiltration and fibrotic changes. Finally, ST2 treatment markedly lowered the levels of IL-4, IL-6, IL-13, IL-33, monocyte chemoattractant protein-1, and transforming growth factor-β1, whereas it increased the levels of interferon-γ in bronchoalveolar lavage fluid. The results indicate that ST2 might prevent bleomycin-induced pulmonary fibrosis possibly through downregulating proinflammatory and profibrotic mediators. This study suggests that lentivirus expressing soluble ST2 might represent an effective therapeutic approach in the treatment of pulmonary fibrotic diseases.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: International Immunopharmacology - Volume 30, January 2016, Pages 188–193
نویسندگان
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