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10.1111/ajt.13690 http://scihub22266oqcxt.onion/10.1111/ajt.13690 C4879508!4879508 !26714197     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26714197 &cmd=llinks): Failed to open stream: HTTP request failed! 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Pseudomonas aeruginosa Induced Airway Epithelial Injury Drives Fibroblast Activation: A Mechanism in Chronic Lung Allograft Dysfunction |pdf=|usr=}}{{26714197 }} gab.com Text Pseudomonas aeruginosa Induced Airway Epithelial Injury Drives Fibroblast Activation: A Mechanism in Chronic Lung Allograft Dysfunction JO: Am J Transplant http://www.kidney.de/pget.php?&tw=1&pmid=26714197 #FOAvip Bacterial infections after lung transplantation cause airway epithelial injury and are associated with an increased risk of developing bronchiolitis obliterans syndrome. The damaged epithelium is a source of alarmins that activate the innate immune system, yet their ability to activate fibroblasts in the development of bronchiolitis obliterans syndrome has not been evaluated. Two epithelial alarmins were measured longitudinally in bronchoalveolar lavages from lung transplant recipients who developed bronchiolitis obliterans syndrome and were compared to stable controls. In addition, conditioned media from human airway epithelial cells infected with Pseudomonas aeruginosa was applied to lung fibroblasts and inflammatory responses were determined. Interleukin-1 alpha (IL-1?) was increased in bronchoalveolar lavage of lung transplant recipients growing P. aeruginosa (11.5 [5.4-21.8] vs. 2.8 [0.9-9.4] pg/mL, p < 0.01) and was significantly elevated within 3 months of developing bronchiolitis obliterans syndrome (8.3 [1.4-25.1] vs. 3.6 [0.6-17.1] pg/mL, p < 0.01), whereas high mobility group protein B1 remained unchanged. IL-1? positively correlated with elevated bronchoalveolar lavage IL-8 levels (r(2)  = 0.6095, p < 0.0001) and neutrophil percentage (r(2)  = 0.25, p = 0.01). Conditioned media from P. aeruginosa infected epithelial cells induced a potent pro-inflammatory phenotype in fibroblasts via an IL-1?/IL-1R-dependent signaling pathway. In conclusion, we propose that IL-1? may be a novel therapeutic target to limit Pseudomonas associated allograft injury after lung transplantation. Twit Text FOAVip Pseudomonas aeruginosa Induced Airway Epithelial Injury Drives Fibroblast Activation: A Mechanism in Chronic Lung Allograft Dysfunction ????Am J Transplant http://www.kidney.de/pget.php?&tw=1&pmid=26714197 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26714197 #FOAvip English Wikipedia <ref>{{Cite pmid|26714197 }}</ref> Pseudomonas aeruginosa Induced Airway Epithelial Injury Drives Fibroblast Activation: A Mechanism in Chronic Lung Allograft Dysfunction #MMPMID26714197 Borthwick LA ; Suwara MI ; Carnell SC ; Green NJ ; Mahida R ; Dixon D ; Gillespie CS ; Cartwright TN ; Horabin J ; Walker A ; Olin E ; Rangar M ; Gardner A ; Mann J ; Corris PA ; Mann DA ; Fisher AJ Am J Transplant 2016[Jun]; 16 (6 ): 1751-65 PMID26714197 show ga Bacterial infections after lung transplantation cause airway epithelial injury and are associated with an increased risk of developing bronchiolitis obliterans syndrome. The damaged epithelium is a source of alarmins that activate the innate immune system, yet their ability to activate fibroblasts in the development of bronchiolitis obliterans syndrome has not been evaluated. Two epithelial alarmins were measured longitudinally in bronchoalveolar lavages from lung transplant recipients who developed bronchiolitis obliterans syndrome and were compared to stable controls. In addition, conditioned media from human airway epithelial cells infected with Pseudomonas aeruginosa was applied to lung fibroblasts and inflammatory responses were determined. Interleukin-1 alpha (IL-1?) was increased in bronchoalveolar lavage of lung transplant recipients growing P. aeruginosa (11.5 [5.4-21.8] vs. 2.8 [0.9-9.4] pg/mL, p < 0.01) and was significantly elevated within 3 months of developing bronchiolitis obliterans syndrome (8.3 [1.4-25.1] vs. 3.6 [0.6-17.1] pg/mL, p < 0.01), whereas high mobility group protein B1 remained unchanged. IL-1? positively correlated with elevated bronchoalveolar lavage IL-8 levels (r(2)  = 0.6095, p < 0.0001) and neutrophil percentage (r(2)  = 0.25, p = 0.01). Conditioned media from P. aeruginosa infected epithelial cells induced a potent pro-inflammatory phenotype in fibroblasts via an IL-1?/IL-1R-dependent signaling pathway. In conclusion, we propose that IL-1? may be a novel therapeutic target to limit Pseudomonas associated allograft injury after lung transplantation. |Acute Lung Injury/*etiology/pathology [MESH] |Adult [MESH] |Allografts [MESH] |Bronchiolitis Obliterans/*etiology/pathology [MESH] |Bronchoalveolar Lavage Fluid [MESH] |Epithelial Cells/immunology/*microbiology/pathology [MESH] |Female [MESH] |Fibroblasts/*pathology [MESH] |Graft Rejection/*etiology/pathology [MESH] |Humans [MESH] |Inflammation/etiology/pathology [MESH] |Interleukin-1alpha/immunology [MESH] |Lung Transplantation/*adverse effects [MESH] |Male [MESH] |Middle Aged [MESH] |Neutrophils/immunology [MESH] |Pseudomonas Infections/complications/microbiology [MESH] |Pseudomonas aeruginosa/*pathogenicity [MESH] |Respiratory Mucosa/immunology/*microbiology/pathology [MESH] |Retrospective Studies [MESH]Pseudomonas aeruginosa Induced Airway Epithelial Injury Drives Fibrobl(epmc).pdf DeepDyve Pubget Overpricing