Dysregulated Lung Commensal Bacteria Drive Interleukin-17B Production to Promote Pulmonary Fibrosis through Their Outer Membrane Vesicles
文献类型：期刊论文
| 作者 | Yang, Daping8; Wang, Jingjing8; Lou, Qi8; Lou, Yunwei8; Qian, Youcun8; Qian, Youcun7; Chen, Xi1; Li, Li2,3; Wang, Honglin4; Wu, Meng4 |
| 刊名 | IMMUNITY
 |
| 出版日期 | 2019 |
| 卷号 | 50期号:3页码:692-+ |
| ISSN号 | 1074-7613 |
| 关键词 | Tfeb Akt signalling Phosphorylation Oxidative stress SH-SY5Y cell Neuronal apoptosis |
| DOI | 10.1016/j.immuni.2019.02.001 |
| 文献子类 | Article |
| 英文摘要 | Idiopathic pulmonary fibrosis (IPF) is a severe form of lung fibrosis with a high mortality rate. However, the etiology of IPF remains unknown. Here, we report that alterations in lung microbiota critically promote pulmonary fibrosis pathogenesis. We found that lung microbiota was dysregulated, and the dysregulated microbiota in turn induced production of interleukin-17B (IL-17B) during bleomycin-induced mouse lung fibrosis. Either lung-microbiota depletion or IL-17B deficiency ameliorated the disease progression. IL-17B cooperated with tumor necrosis factor-a to induce expression of neutrophil-recruiting genes and T helper 17 (Th17)-cell-promoting genes. Three pulmonary commensal microbes, which belong to the genera Bacteroides and Prevotella, were identified to promote fibrotic pathogenesis through IL-17R signaling. We further defined that the outer membrane vesicles (OMVs) that were derived from the identified commensal microbes induced IL-17B production through Toll-like receptor-Myd88 adaptor signaling. Together our data demonstrate that specific pulmonary symbiotic commensals can promote lung fibrosis by regulating a profibrotic inflammatory cytokine network. |
| 学科主题 | Immunology |
| WOS关键词 | AIRWAY INFLAMMATION ; IL-17 ; CELLS ; GUT ; MICROBIOME ; RECEPTOR ; BIOGENESIS ; MECHANISMS ; EXPRESSION ; BLEOMYCIN |
| 语种 | 英语 |
| 出版者 | CELL PRESS |
| WOS记录号 | WOS:000461660500019 |
| 版本 | 出版稿 |
| 源URL | [http://202.127.25.144/handle/331004/856]  |
| 专题 | 中国科学院上海生命科学研究院营养科学研究所 |
| 作者单位 | 1.Shanghai Jiao Tong Univ, Int Peace Matern & Child Hlth Hosp, Sch Med, Shanghai 200030, Peoples R China; 2.Shanghai Univ Tradit Chinese Med, Shuguang Hosp, Dept Resp Dis, Baoshan Branch, Shanghai 201900, Peoples R China; 3.Baoshan Dist Hosp Integrated Tradit Chinese & Wes, Dept Resp Dis, Shanghai 201900, Peoples R China; 4.Shanghai Jiao Tong Univ, Shanghai Inst Immunol, Inst Med Sci, Sch Med, Shanghai 200025, Peoples R China; 5.Chinese Acad Sci, Inst Biochem & Cell Biol, Shanghai Inst Biol Sci, State Key Lab Mol Biol, Shanghai 200031, Peoples R China; 6.Harvard Med Sch, Dept Immunol, Boston, MA 02115 USA, 7.ShanghaiTech Univ, Sch Life Sci & Technol, Shanghai 200031, Peoples R China; 8.Univ Chinese Acad Sci, Chinese Acad Sci, Shanghai Inst Biol Sci,CAS Ctr Excellence Mol Cel, Shanghai Inst Nutr & Hlth,CAS Key Lab Tissue Micr, Shanghai 200031, Peoples R China; |
| 推荐引用方式 GB/T 7714 | Yang, Daping,Wang, Jingjing,Lou, Qi,et al. Dysregulated Lung Commensal Bacteria Drive Interleukin-17B Production to Promote Pulmonary Fibrosis through Their Outer Membrane Vesicles[J]. IMMUNITY,2019,50(3):692-+. |
| APA | Yang, Daping.,Wang, Jingjing.,Lou, Qi.,Lou, Yunwei.,Qian, Youcun.,...&,.(2019).Dysregulated Lung Commensal Bacteria Drive Interleukin-17B Production to Promote Pulmonary Fibrosis through Their Outer Membrane Vesicles.IMMUNITY,50(3),692-+. |
| MLA | Yang, Daping,et al."Dysregulated Lung Commensal Bacteria Drive Interleukin-17B Production to Promote Pulmonary Fibrosis through Their Outer Membrane Vesicles".IMMUNITY 50.3(2019):692-+. |
入库方式： OAI收割
来源：上海营养与健康研究所
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