Dysregulated Lung Commensal Bacteria Drive Interleukin-17B Production to Promote Pulmonary Fibrosis through Their Outer Membrane Vesicles

doi:10.1016/j.immuni.2019.02.001

	Dysregulated Lung Commensal Bacteria Drive Interleukin-17B Production to Promote Pulmonary Fibrosis through Their Outer Membrane Vesicles
	Yang, Daping 1; Chen, Xi 3; Wang, Jingjing 1; Lou, Qi 1; Lou, Yunwei 1; Li, Li 4,5; Wang, Honglin 6; Chen, Jiangye 7; Wu, Meng 6; Song, Xinyang 8; Qian, Youcun1,2
	2019-03-19
发表期刊	IMMUNITY (IF:25.5[JCR-2023],33.2[5-Year])
ISSN	1074-7613
卷号	50 期号:3 页码:692-+
发表状态	已发表
DOI	10.1016/j.immuni.2019.02.001
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.
收录类别	SCI ; SCIE
语种	英语
资助项目	Strategic Priority Research Program of the Chinese Academy of Sciences[XDB19000000]
WOS研究方向	Immunology
WOS类目	Immunology
WOS记录号	WOS:000461660500019
出版者	CELL PRESS
WOS关键词	AIRWAY INFLAMMATION ; IL-17 ; CELLS ; GUT ; MICROBIOME ; RECEPTOR ; BIOGENESIS ; MECHANISMS ; EXPRESSION ; BLEOMYCIN
原始文献类型	Article
引用统计	正在获取...
文献类型	期刊论文
条目标识符	https://kms.shanghaitech.edu.cn/handle/2MSLDSTB/30614
专题	生命科学与技术学院_特聘教授组_钱友存组
通讯作者	Qian, Youcun
作者单位	1.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 2.ShanghaiTech Univ, Sch Life Sci & Technol, Shanghai 200031, Peoples R China 3.Shanghai Jiao Tong Univ, Int Peace Matern & Child Hlth Hosp, Sch Med, Shanghai 200030, Peoples R China 4.Shanghai Univ Tradit Chinese Med, Shuguang Hosp, Dept Resp Dis, Baoshan Branch, Shanghai 201900, Peoples R China 5.Baoshan Dist Hosp Integrated Tradit Chinese & Wes, Dept Resp Dis, Shanghai 201900, Peoples R China 6.Shanghai Jiao Tong Univ, Shanghai Inst Immunol, Inst Med Sci, Sch Med, Shanghai 200025, Peoples R China 7.Chinese Acad Sci, Inst Biochem & Cell Biol, Shanghai Inst Biol Sci, State Key Lab Mol Biol, Shanghai 200031, Peoples R China 8.Harvard Med Sch, Dept Immunol, Boston, MA 02115 USA
通讯作者单位	生命科学与技术学院
推荐引用方式 GB/T 7714	Yang, Daping,Chen, Xi,Wang, Jingjing,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.,Chen, Xi.,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-+.