Journal
AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY
Volume 294, Issue 6, Pages L1035-L1042Publisher
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajplung.00397.2007
Keywords
lung; matrix metalloproteinases; collectin
Categories
Funding
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL059215, K08HL077138, K08HL071607] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE ON AGING [R37AG015052, R01AG015052] Funding Source: NIH RePORTER
- NHLBI NIH HHS [K08 HL071607, K08 HL077138, K08-HL-077138, K08-HL-071607, R01 HL059215, HL-59215] Funding Source: Medline
- NIA NIH HHS [R37 AG015052, AG-15052, R01 AG015052] Funding Source: Medline
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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.
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