NDLI: Resolvin D1 attenuates polyinosinic-polycytidylic acid-induced inflammatory signaling in human airway epithelial cells via TAK1.

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Resolvin D1 attenuates polyinosinic-polycytidylic acid-induced inflammatory signaling in human airway epithelial cells via TAK1.

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Resolvin D1 attenuates polyinosinic-polycytidylic acid-induced inflammatory signaling in human airway epithelial cells via TAK1.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Levy, Elizabeth P. Owens, Kristina M. Phipps, Richard P. Sime, Patricia J. Fulton, Robert A. Thatcher, Thomas H. Hsiao, Hsi-Min
Description	Author Affiliation: Hsiao HM ( Department of Pathology and Laboratory Medicine, University of Rochester School of Medicine and Dentistry, Rochester, NY 14642); Thatcher TH ( Lung Biology and Disease Program, University of Rochester School of Medicine and Dentistry, Rochester, NY 14642); Levy EP ( Lung Biology and Disease Program, University of Rochester School of Medicine and Dentistry, Rochester, NY 14642); Fulton RA ( Lung Biology and Disease Program, University of Rochester School of Medicine and Dentistry, Rochester, NY 14642); Owens KM ( Division of Pulmonary and Critical Care Medicine, Department of Medicine, University of Rochester School of Medicine and Dentistry, Rochester, NY 14642); Phipps RP ( Lung Biology and Disease Program, University of Rochester School of Medicine and Dentistry, Rochester, NY 14642); Sime PJ ( Lung Biology and Disease Program, University of Rochester School of Medicine and Dentistry, Rochester, NY 14642)
Abstract	The respiratory epithelium consists of lung sentinel cells, which are the first to contact inhaled inflammatory insults, including air pollutants, smoke, and microorganisms. To avoid damaging exuberant or chronic inflammation, the inflammatory process must be tightly controlled and terminated once the insult is mitigated. Inflammation resolution is now known to be an active process involving a new genus of lipid mediators, called 'specialized proresolving lipid mediators,' that includes resolvin D1 (RvD1). We and others have reported that RvD1 counteracts proinflammatory signaling and promotes resolution. A knowledge gap is that the specific cellular targets and mechanisms of action for RvD1 remain largely unknown. In this article, we identified the mechanism whereby RvD1 disrupts inflammatory mediator production induced by the viral mimic polyinosinic-polycytidylic acid [poly(I:C)] in primary human lung epithelial cells. RvD1 strongly suppressed the viral mimic poly(I:C)-induced IL-6 and IL-8 production and proinflammatory signaling involving MAPKs and NF-κB. Most importantly, we found that RvD1 inhibited the phosphorylation of TAK1 (TGF-ß-activated kinase 1), a key upstream regulatory kinase common to both the MAPK and NF-κB pathways, by inhibiting the formation of a poly(I:C)-induced signaling complex composed of TAK1, TAB1 (TAK1 binding protein), and TRAF6 (TNF receptor-associated factor 6). We confirmed that ALX/FPR2 and GPR32, two RvD1 receptors, were expressed on human small airway epithelial cells. Furthermore, blocking these receptors abrogated the inhibitory action of RvD1. In this article, we present the idea that RvD1 has the potential to be used as an anti-inflammatory and proresolving agent, possibly in the context of exuberant host responses to damaging respirable agents such as viruses.
ISSN	00221767
e-ISSN	15506606
DOI	10.4049/jimmunol.1400313
Journal	The Journal of Immunology
Issue Number	10
Volume Number	193
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2014-11-15
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Docosahexaenoic Acids Immunology Epithelial Cells Drug Effects Map Kinase Kinase Kinases Poly I-c Pharmacology Adaptor Proteins, Signal Transducing Antagonists & Inhibitors Genetics Bronchi Pathology Gene Expression Regulation Inflammation Interleukin-6 Biosynthesis Interleukin-8 Mitogen-activated Protein Kinases Nf-kappa B Primary Cell Culture Rna, Small Interfering Receptors, G-protein-coupled Signal Transduction Tnf Receptor-associated Factor 6 Research Support, N.i.h., Extramural Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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