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10.1165/rcmb.2016-0259OC http://scihub22266oqcxt.onion/10.1165/rcmb.2016-0259OC C5449514!5449514 !27911568     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27911568 &cmd=llinks): Failed to open stream: HTTP request failed! 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NF-?B Mediates Mesenchymal Transition, Remodeling, and Pulmonary Fibrosis in Response to Chronic Inflammation by Viral RNA Patterns |pdf=|usr=}}{{27911568 }} gab.com Text NF- B Mediates Mesenchymal Transition, Remodeling, and Pulmonary Fibrosis in Response to Chronic Inflammation by Viral RNA Patterns JO: Am J Respir Cell Mol Biol http://www.kidney.de/pget.php?&tw=1&pmid=27911568 #FOAvip Airway remodeling is resultant of a complex multicellular response associated with a progressive decline of pulmonary function in patients with chronic airway disease. Here, repeated infections with respiratory viruses are linked with airway remodeling through largely unknown mechanisms. Although acute activation of the Toll-like receptor (TLR) 3 pathway by extracellular polyinosinic:polycytidylic acid (poly[I:C]) induces innate signaling through the NF-?B transcription factor in normal human small airway epithelial cells, prolonged (repetitive or tonic) poly(I:C) stimulation produces chronic stress fiber formation, mesenchymal transition, and activation of a fibrotic program. Chronic poly(I:C) stimulation enhanced the expression of core mesenchymal regulators Snail family zinc finger 1, zinc finger E-box binding homeobox, mesenchymal intermediate filaments (vimentin), and extracellular matrix proteins (fibronectin-1), and collagen 1A. This mesenchymal transition was prevented by silencing expression of NF-?B/RelA or administration of a small-molecule inhibitor of the I?B kinase, BMS345541. Acute poly(I:C) exposure in vivo induced profound neutrophilic airway inflammation. When administered repetitively, poly(I:C) resulted in enhanced fibrosis observed by lung micro-computed tomography, second harmonic generation microscopy of optically cleared lung tissue, and by immunohistochemistry. Epithelial flattening, expansion of the epithelial mesenchymal trophic unit, and enhanced Snail family zinc finger 1 and fibronectin 1 expression in airway epithelium were also observed. Repetitive poly(I:C)-induced airway remodeling, fibrosis, and epithelial-mesenchymal transition was inhibited by BMS345541 administration. Based on this novel model of viral inflammation-induced remodeling, we conclude that NF-?B is a major controller of epithelial-mesenchymal transition and pulmonary fibrosis, a finding that has potentially important relevance to airway remodeling produced by repetitive viral infections. Twit Text FOAVip NF- B Mediates Mesenchymal Transition, Remodeling, and Pulmonary Fibrosis in Response to Chronic Inflammation by Viral RNA Patterns ????Am J Respir Cell Mol Biol http://www.kidney.de/pget.php?&tw=1&pmid=27911568 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27911568 #FOAvip English Wikipedia <ref>{{Cite pmid|27911568 }}</ref> NF-?B Mediates Mesenchymal Transition, Remodeling, and Pulmonary Fibrosis in Response to Chronic Inflammation by Viral RNA Patterns #MMPMID27911568 Tian B ; Patrikeev I ; Ochoa L ; Vargas G ; Belanger KK ; Litvinov J ; Boldogh I ; Ameredes BT ; Motamedi M ; Brasier AR Am J Respir Cell Mol Biol 2017[Apr]; 56 (4 ): 506-520 PMID27911568 show ga Airway remodeling is resultant of a complex multicellular response associated with a progressive decline of pulmonary function in patients with chronic airway disease. Here, repeated infections with respiratory viruses are linked with airway remodeling through largely unknown mechanisms. Although acute activation of the Toll-like receptor (TLR) 3 pathway by extracellular polyinosinic:polycytidylic acid (poly[I:C]) induces innate signaling through the NF-?B transcription factor in normal human small airway epithelial cells, prolonged (repetitive or tonic) poly(I:C) stimulation produces chronic stress fiber formation, mesenchymal transition, and activation of a fibrotic program. Chronic poly(I:C) stimulation enhanced the expression of core mesenchymal regulators Snail family zinc finger 1, zinc finger E-box binding homeobox, mesenchymal intermediate filaments (vimentin), and extracellular matrix proteins (fibronectin-1), and collagen 1A. This mesenchymal transition was prevented by silencing expression of NF-?B/RelA or administration of a small-molecule inhibitor of the I?B kinase, BMS345541. Acute poly(I:C) exposure in vivo induced profound neutrophilic airway inflammation. When administered repetitively, poly(I:C) resulted in enhanced fibrosis observed by lung micro-computed tomography, second harmonic generation microscopy of optically cleared lung tissue, and by immunohistochemistry. Epithelial flattening, expansion of the epithelial mesenchymal trophic unit, and enhanced Snail family zinc finger 1 and fibronectin 1 expression in airway epithelium were also observed. Repetitive poly(I:C)-induced airway remodeling, fibrosis, and epithelial-mesenchymal transition was inhibited by BMS345541 administration. Based on this novel model of viral inflammation-induced remodeling, we conclude that NF-?B is a major controller of epithelial-mesenchymal transition and pulmonary fibrosis, a finding that has potentially important relevance to airway remodeling produced by repetitive viral infections. |*Airway Remodeling/drug effects [MESH] |*Epithelial-Mesenchymal Transition/drug effects [MESH] |Animals [MESH] |Bronchoalveolar Lavage Fluid [MESH] |Chronic Disease [MESH] |Collagen/metabolism [MESH] |Epithelial Cells/drug effects/metabolism/pathology [MESH] |Humans [MESH] |Lung/pathology [MESH] |Mesoderm/drug effects/*pathology [MESH] |Mice, Inbred C57BL [MESH] |NF-kappa B/*metabolism [MESH] |Neutrophils/pathology [MESH] |Pneumonia/complications/diagnostic imaging/*pathology/*physiopathology [MESH] |Poly I-C/pharmacology [MESH] |Pulmonary Fibrosis/complications/metabolism/pathology/*physiopathology [MESH] |RNA, Viral/*pharmacology [MESH] |Signal Transduction/drug effects [MESH] |Toll-Like Receptor 3/metabolism [MESH]NF-?B Mediates Mesenchymal Transition, Remodeling, and Pulmonary Fibro(epmc).pdf DeepDyve Pubget Overpricing