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- Title
A Recombinant Fragment of Human Surfactant Protein D Reduces Alveolar Macrophage Apoptosis and Pro-Inflammatory Cytokines in Mice Developing Pulmonary Emphysema.
- Authors
CLARK, HOWARD; PALANIYAR, NADES; HAWGOOD, SAMUEL; REID, KENNETH B M.
- Abstract
Rapid removal of apoptotic cells is an important mechanism for immune homeostasis and the resolution of inflammation. Delayed clearance of apoptotic alveolar macrophages may cause activation of healthy bystander macrophages and contribute to high macrophage number and emphysema in surfactant protein D (SP-D) knock-out mice. Using flow cytometry and Annexin V and propidium iodide as markers for apoptosis and necrosis, respectively, SP-D-deficient mice were found to have a 5- to 10-fold increase in the number of apoptotic and necrotic alveolar macrophages in the lungs. SP-D-deficient mice accumulate apoptotic macrophages in the lung, and this accumulation can be reduced by treatment with recombinant SP-D (but not SP-A). The recombinant SP-D binds preferentially to apoptotic cells. The data are consistent with a specific role in vivo for SP-D in promoting apoptotic cell clearance in the lungs to limit macrophage-mediated inflammation and reveal a potential new mechanism for therapeutic targeting in the prevention of emphysema.
- Subjects
APOPTOSIS; KILLER cells; LABORATORY mice; PULMONARY emphysema; IMMUNOCOMPETENT cells; MACROPHAGES; CELL death; PHYSIOLOGICAL control systems; INFLAMMATION
- Publication
Annals of the New York Academy of Sciences, 2004, Vol 1010, Issue 1, p113
- ISSN
0077-8923
- Publication type
Article
- DOI
10.1196/annals.1299.019