Alveolar macrophage activation and an emphysema-like phenotype in adiponectin-deficient mice.
Publication/Presentation Date
6-1-2008
Abstract
Adiponectin is an adipocyte-derived collectin that acts on a wide range of tissues including liver, brain, heart, and vascular endothelium. To date, little is known about the actions of adiponectin in the lung. Herein, we demonstrate that adiponectin is present in lung lining fluid and that adiponectin deficiency leads to increases in proinflammatory mediators and an emphysema-like phenotype in the mouse lung. Alveolar macrophages from adiponectin-deficient mice spontaneously display increased production of tumor necrosis factor-alpha (TNF-alpha) and matrix metalloproteinase (MMP-12) activity. Consistent with these observations, we found that pretreatment of alveolar macrophages with adiponectin leads to TNF-alpha and MMP-12 suppression. Together, our findings show that adiponectin leads to macrophage suppression in the lung and suggest that adiponectin-deficient states may contribute to the pathogenesis of inflammatory lung conditions such as emphysema.
Volume
294
Issue
6
First Page
1035
Last Page
1042
ISSN
1040-0605
Published In/Presented At
Summer, R., Little, F. F., Ouchi, N., Takemura, Y., Aprahamian, T., Dwyer, D., Fitzsimmons, K., Suki, B., Parameswaran, H., Fine, A., & Walsh, K. (2008). Alveolar macrophage activation and an emphysema-like phenotype in adiponectin-deficient mice. American journal of physiology. Lung cellular and molecular physiology, 294(6), L1035–L1042. https://doi.org/10.1152/ajplung.00397.2007
Disciplines
Business Administration, Management, and Operations | Health and Medical Administration | Management Sciences and Quantitative Methods
PubMedID
18326826
Department(s)
Administration and Leadership
Document Type
Article