BioProject

To further understand the early molecular events in antibody mediated chronic inflammation of the lungs, we utilized a murine Obliterative Airway Disease (OAD) model of native lungs where Abs to MHC class I induces bronchiolar obliteration and fibrosis. More...

To further understand the early molecular events in antibody mediated chronic inflammation of the lungs, we utilized a murine Obliterative Airway Disease (OAD) model of native lungs where Abs to MHC class I induces bronchiolar obliteration and fibrosis. This study identified a unique transcriptional profile with a set of genes that were stimulated while another set of genes that were repressed in anti MHC I treated lungs compared to that of isotype treated lungs. Lung transplantation (LTx) is an accepted clinical intervention for various intractable pulmonary dysfunctions. However, de novo Abs to mismatched donor HLA (DSA) predispose lung-grafts to chronic rejection, Bronchiolitis Obliterans Syndrome (BOS). The anti-MHC induced mouse OAD model, the only available preclinical model for study of early pathogenesis following MHC ligation, produces lesions analogous to BOS. Overall design: Induction of gene expression was measured following intrabronchial administration of anti-MHC class I (H-2Kb) Ab at 200μg/mouse. Samples were collected on days 1, 2, 3 and 6 post-Ab administration. Isotype matched control Ab was administered at an equivalent dose and gene expression profile in isotype treated group served as the base line expression and was compared with that of anti-H-2Kb treated group. A total of 24 samples were processed with two treatment groups (anti-H-2Kb, isotype), four time points (days 1, 2, 3 and 6) and three biological replicates. Less...