About Us
The Department of Genetic Medicine at Weill Cornell leads a dynamic and innovative translational research program, advancing diverse fields such as Genetic Therapy and Personalized Medicine.
The Department of Genetic Medicine at Weill Cornell leads a dynamic and innovative translational research program, advancing diverse fields such as Genetic Therapy and Personalized Medicine.
Our translational research program aims to leverage our expertise in genetic therapies and personalized medicine to develop clinical solutions that target the molecular causes of human diseases.
The Department of Genetic Medicine advances treatments and diagnostics through diverse clinical trials, including drug testing and research to better understand diseases.
The Belfer Gene Therapy Core Facility (BGTCF) is a cutting-edge genetic medicine research facility.
The Department of Genetic Medicine at Weill Cornell leads a dynamic and innovative translational research program, advancing diverse fields such as Genetic Therapy and Personalized Medicine.
Our translational research program aims to leverage our expertise in genetic therapies and personalized medicine to develop clinical solutions that target the molecular causes of human diseases.
The Department of Genetic Medicine advances treatments and diagnostics through diverse clinical trials, including drug testing and research to better understand diseases.
The Belfer Gene Therapy Core Facility (BGTCF) is a cutting-edge genetic medicine research facility.
Publication Type | Academic Article |
Authors | Bernardo J, Hunninghake G, Gadek J, Ferrans V, Crystal R |
Journal | Am Rev Respir Dis |
Volume | 120 |
Issue | 5 |
Pagination | 985-94 |
Date Published | 11/01/1979 |
ISSN | 0003-0805 |
Keywords | Alveolitis, Extrinsic Allergic, Lung, T-Lymphocytes |
Abstract | The earliest lesion in hypersensitivity penumonitis is an acute inflammatory alveolitis characterized by parenchymal hemorrhage and accumulations of polymorphonuclear leukocytes within the lung. In many instances, this initial lesion is replaced by a more chronic alveolitis, with development of mononuclear cell interstitial infiltrate, granuloma formation, and interstitial fibrosis. To help define the mechanisms by which the early polymorphonuclear leukocyte alveolitis of acute hypersensitivity pneumonitis evolves into a chronic mononuclear-cell process, an animal model of the disease was developed using guinea pigs sensitized by footpad injeection with either ovalbumin (OVA) in complete Freund's adjuvant (CFA), CFA alone, or phosphate-buffered saline. Ten days after sensitization, the animals were challenged by intratracheal injection of either particulate OVA, particulate human serum albumin, or phosphate-buffered saline alone, and their lungs were evaluated sequentially for changes in histologic appearance and lymphocyte subpopulations. After challenge, only animals sensitized with CFA plus OVA and challenged with particulate OVA developed pulmonary lesions consistent with acute hypersensitivity pneumonitis. Within 4 h after challenge, these animals developed an acute hemorrhagic alveolitis that persisted for more than 24 h. By 48 to 96 h, the alveolitis evolved into a predominantly mononuclear-cell infiltrate. This change in the histologic appearance of the lungs in these animals was preceded by a rapid increase in the proportions of T-lymphocytes within the lungs, noted by 24 h after intratracheal challenge with specific antigen. Before intratracheal challenge with antigen, lung lymphocytes from only the group of animals immunized with CFA plus OVA were capable of proliferating on exposure to OVA in vitro. In the same group, lymphocytes recovered from the lung after intratracheal particulate OVA demonstrated blast transformation in vivo, a phenomenon not found in any other group. These studies suggest that the alveolitis of acute hypersensitivity pneumonitis is rapidly associated with changes in populations of immune effector cells before development of the mononuclear cell alveolitis characteristic of the chronic disease. |
DOI | 10.1164/arrd.1979.120.5.985 |
PubMed ID | 315742 |