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Pulmonary mechanical and immunologic dysfunction in a murine model of AIDS
C L Hartsfield1, D Lipke, Y L Lai
1Department of Microbiology and Immunology, College of Pharmacy, University of Kentucky, Lexington 40536-0082, USA.
The American Journal of Physiology
|April 1, 1997
Summary
Acquired immunodeficiency syndrome (AIDS) in mice causes lung alveolar septal wall thickening and impaired carbon monoxide diffusion. Activated lung immune cells and cytokines likely mediate these respiratory changes.
Area of Science:
- Pulmonary Medicine
- Immunology
- Pathology
Background:
- Human immunodeficiency virus (HIV)-infected patients may develop lung abnormalities.
- The mechanisms behind these respiratory changes in HIV infection are not fully understood.
Purpose of the Study:
- To investigate lung structural and functional changes in a murine model of acquired immunodeficiency syndrome (AIDS).
- To determine if altered lung lymphocyte deposition and activation contribute to respiratory abnormalities.
Main Methods:
- Evaluation of alveolar septal wall thickness and lung fibronectin/collagen IV deposition.
- Pulmonary function tests (PFTs) including diffusion capacity for carbon monoxide (DLCO).
- Immunohistochemistry, flow cytometry, and RT-PCR analysis of lung tissues and cells.
Main Results:
- Alveolar septal wall thickening was observed 8 weeks post-infection.
- Significant impairment in DLCO was noted in infected mice.
- Increased deposition of fibronectin and collagen IV in septal walls.
- Activated lymphocytes and macrophages, along with increased cytokine mRNA, were found in the lungs.
Conclusions:
- A murine model of AIDS exhibits impaired gas exchange.
- Activated lung immune cells and their secreted cytokines may cause structural and functional lung alterations in AIDS.