UNASSIGNED: @entity2348 after lung transplantation cause airway epithelial injury and are associated with an increased risk of developing @entity4154 . The damaged epithelium is a source of alarmins that activate the innate immune system, yet their ability to activate fibroblasts in the development of @entity4154 has not been evaluated. Two epithelial alarmins were measured longitudinally in bronchoalveolar lavages from lung transplant recipients who developed @entity4154 and compared to stable controls. In addition, conditioned media from @entity1 airway epithelial cells infected with @entity796 , was applied to lung fibroblasts and inflammatory responses determined. IL-1a was increased in bronchoalveolar lavage of lung transplant recipients growing @entity796 (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 @entity4154 (8.3(1.4-25.1) vs 3.6(0.6-17.1) pg/ml, p<0.01) whereas HMGB1 remained unchanged. IL-1a 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 @entity796 infected epithelial cells induced a potent pro-inflammatory phenotype in fibroblasts via an IL-1a/IL-1R dependant signaling pathway. In conclusion, we propose that IL-1a may be a novel therapeutic target to limit @entity796 associated allograft injury after lung transplantation. This article is protected by copyright. All rights reserved.

XXXX induced airway epithelial injury drives fibroblast activation: a mechanism in chronic lung allograft dysfunction.

@entity1 :: ('9606', 'Species') :: ['human'] @entity4154 :: ('MESH:D001989', 'Disease') :: ['bronchiolitis obliterans syndrome'] @entity2348 :: ('MESH:D001424', 'Disease') :: ['Bacterial infections'] @entity796 :: ('287', 'Species') :: ['Pseudomonas aeruginosa', 'Pseudomonas']
@entity796 :: (287,Species) :: ['Pseudomonas aeruginosa']
