Recommended Reading from Cedars-Sinai Medical Center Fellows
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|Title:||Recommended Reading from Cedars-Sinai Medical Center Fellows||Authors:||Coyle Rowan, Simon; Bora, Stephanie; Burman, Ankita; Xie, Ting||Permanent link:||http://hdl.handle.net/10197/10944||Date:||2-Jul-2019||Online since:||2019-07-24T09:04:13Z||Abstract:||Idiopathic pulmonary fibrosis (IPF) is a severe disease with no cure, and a median survival rate of < 5 years (1). Other research indicates the cytokine IL-17 is part of the pro-fibrotic inflammatory response (2). The critical influence of the gut microbiome in IL-17 immune responses has been established (3), yet the role of the lung microbiota in lung inflammation, and specifically IL-17 responses that promote IPF, is overlooked. In their Immunity paper, Yang et al used the bleomycin model of fibrosis to determine if IL-17B, one of six IL-17 cytokines, caused lung fibrosis, and if the lung microbiome regulated pro-fibrotic IL-17 production.||Type of material:||Review||Publisher:||American Thoracic Society||Journal:||American Journal of Respiratory Cell and Molecular Biology||Copyright (published version):||2019 American Thoracic Society||Keywords:||Idiopathic pulmonary fibrosis (IPF); Microbiome; Inflammatory; Lung||DOI:||10.1165/rcmb.2019-0196ro||Language:||en||Status of Item:||Peer reviewed|
|Appears in Collections:||Medicine Research Collection|
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