NDLI: Adiponectin attenuates lipopolysaccharide-induced acute lung injury through suppression of endothelial cell activation.

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Adiponectin attenuates lipopolysaccharide-induced acute lung injury through suppression of endothelial cell activation.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Little, Frederic F. Li, Stephanie Z. Denzel, Martin Fine, Alan Konter, Jason M. Ranscht, Barbara Walsh, Kenneth Ouchi, Noriyuki Parker, Jennifer L. Summer, Ross S. Baez, Elizabeth Nakamura, Kazuto
Description	Country affiliation: United States Author Affiliation: Konter JM ( Pulmonary Center, Boston University School of Medicine, Boston, MA 02118, USA.)
Abstract	Adiponectin (APN) is an adipose tissue-derived factor with anti-inflammatory and vascular protective properties whose levels paradoxically decrease with increasing body fat. In this study, APN's role in the early development of ALI to LPS was investigated. Intratracheal LPS elicited an exaggerated systemic inflammatory response in APN-deficient (APN(-/-)) mice compared with wild-type (wt) littermates. Increased lung injury and inflammation were observed in APN(-/-) mice as early as 4 h after delivery of LPS. Targeted gene expression profiling performed on immune and endothelial cells isolated from lung digests 4 h after LPS administration showed increased proinflammatory gene expression (e.g., IL-6) only in endothelial cells of APN(-/-) mice when compared with wt mice. Direct effects on lung endothelium were demonstrated by APN's ability to inhibit LPS-induced IL-6 production in primary human endothelial cells in culture. Furthermore, T-cadherin-deficient mice that have significantly reduced lung airspace APN but high serum APN levels had pulmonary inflammatory responses after intratracheal LPS that were similar to those of wt mice. These findings indicate the importance of serum APN in modulating LPS-induced ALI and suggest that conditions leading to hypoadiponectinemia (e.g., obesity) predispose to development of ALI through exaggerated inflammatory response in pulmonary vascular endothelium.
ISSN	00221767
e-ISSN	15506606
DOI	10.4049/jimmunol.1100426
Journal	The Journal of Immunology
Issue Number	2
Volume Number	188
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2012-01-15
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Acute Lung Injury Immunology Prevention & Control Endothelium, Vascular Pathology Immune Tolerance Lipopolysaccharides Toxicity Metabolism Adiponectin Blood Deficiency Physiology Animals Cadherins Genetics Cell Line, Tumor Cells, Cultured Disease Models, Animal Inflammation Interleukin-6 Antagonists & Inhibitors Biosynthesis Intubation, Intratracheal Lung Blood Supply Mice Mice, Inbred C57bl Mice, Knockout Pulmonary Artery Research Support, N.i.h., Extramural Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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