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EDITORIAL FOCUS

Alveolar macrophage activation and an emphysema-like phenotype in adiponectin-deficient mice

¹The Pulmonary Center, Boston University School of Medicine, ²Whitaker Cardiovascular Institute, Molecular Cardiology/Whitaker Cardiovascular Institute, Boston University School of Medicine, and ³Department of Biomedical Engineering, Boston University, Boston, Massachusetts

Submitted 24 September 2007 ; accepted in final form 7 March 2008

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- (TNF-) and matrix metalloproteinase (MMP-12) activity. Consistent with these observations, we found that pretreatment of alveolar macrophages with adiponectin leads to TNF- 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.

lung; matrix metalloproteinases; collectin

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