資料載入中.....
|
請使用永久網址來引用或連結此文件:
https://ir.lib.ncu.edu.tw/handle/987654321/105768
|
| 題名: | DcR3 suppresses influenza virus-induced macrophage activation and attenuates pulmonary inflammation and lethality |
| 作者: | 吳忻怡;Huang, Ming-Ting;Chen, Szu-Ting;Wu, Hsin-Yi;Chen, Yu-Ju;Chou, Teh-Ying;Hsieh, Shie-Liang |
| 貢獻者: | 總教學中心通識教育中心 |
| 關鍵詞: | Animals;Biomedical and Life Sciences;Biomedicine;Bronchoalveolar Lavage Fluid - cytology;Bronchoalveolar Lavage Fluid - immunology;Cytokines - immunology;Heparan Sulfate Proteoglycans - genetics;Human Genetics;Humans;Immunoglobulin G - pharmacology;Influenza A virus;Internal Medicine;Lung - virology;Macrophage Activation - immunology;Mice, Inbred C57BL;Mice, Transgenic;Mitogen-Activated Protein Kinases - immunology;Molecular Medicine;Original Article;Orthomyxoviridae Infections - immunology;Pneumonia - immunology;Protein Structure, Tertiary;Receptors, Tumor Necrosis Factor, Member 6b - genetics;Receptors, Tumor Necrosis Factor, Member 6b - immunology;Recombinant Fusion Proteins - pharmacology;Toll-Like Receptors - immunology |
| 日期: | 2015-10-03 |
| 上傳時間: | 2026-04-23 12:52:41 (UTC+8) |
| 出版者: | Springer Verlag;Berlin/Heidelberg: Springer Berlin Heidelberg |
| 摘要: | 摘要： Influenza A virus (IAV) infects macrophages and stimulates innate immunity receptors and sensors to produce proinflammatory cytokines and chemokines, which are responsible for IAV-induced pulmonary inflammation and injury. Decoy receptor 3 (DcR3) is a soluble protein belonging to the tumor necrosis factor receptor superfamily (TNFRSF), and is able to skew macrophage differentiation into an M2 phenotype. We demonstrated that DcR3 attenuated IAV-induced secretion of proinflammatory cytokines and chemokine from macrophages, and mitigated pulmonary infiltration and reduce lethality. Proteome-wide phosphoproteomic mapping revealed that DcR3 not only activated STK10, a negative regulator of cell migration, but also inactivated PKC-α, which are crucial for the activation of ERK and JNK in human macrophages. Furthermore, less pulmonary infiltration with lower levels of proinflammatory cytokines and chemokine in bronchoalveolar lavage fluid (BALF) were observed in DcR3-transgenic mice. Moreover, recombinant DcR3.Fc and heparan sulfate proteoglycan binding domain of DcR3.Fc (HBD.Fc) fusion proteins attenuated weight loss and protected mice from IAV-induced lethality. Thus, DcR3-mediated protection is not only via suppression of proinflammatory cytokine and chemokine release, but also via activation of STK10 to inhibit cell infiltration. DcR3 fusion proteins may become therapeutic agents to protect host from IAV-induced lethality in the future. Key message • DcR3 suppresses IAV-induced cytokine secretion. • DcR3 inhibits IAV-induced JNK and ERK activation in human macrophages. • DcR3 downregulates TLR3 and 7 expressions in human macrophages. • DcR3 protects mice from IAV-induced lethality.
其他題名： J Mol Med
其他題名： J Mol Med (Berl)
出版者： Berlin/Heidelberg: Springer Berlin Heidelberg
出版日期： 2015-10-01
出處： Journal of molecular medicine (Berlin, Germany), 2015-10, Vol.93 (10), p.1131-1143
版權： Springer-Verlag Berlin Heidelberg 2015
識別號： ISSN: 0946-2716
識別號： ISSN: 1432-1440
識別號： EISSN: 1432-1440
識別號： DOI: 10.1007/s00109-015-1291-1
識別號： PMID: 25940317 |
| 顯示於類別: | [通識教育中心] 期刊論文
|
文件中的檔案:
| 檔案 |
描述 |
大小 | 格式 | 瀏覽次數 |
|---|
| index.html | | 0Kb | HTML | 34 | 檢視/開啟 |
|
在NCUIR中所有的資料項目都受到原著作權保護.
|
