NDLI: The phosphoinositide 3-kinase-dependent activation of Btk is required for optimal eicosanoid production and generation of reactive oxygen species in antigen-stimulated mast cells

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The phosphoinositide 3-kinase-dependent activation of Btk is required for optimal eicosanoid production and generation of reactive oxygen species in antigen-stimulated mast cells

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The phosphoinositide 3-kinase-dependent activation of Btk is required for optimal eicosanoid production and generation of reactive oxygen species in antigen-stimulated mast cells

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Beaven, Michael A. Gilfillan, Alasdair M. Swindle, Emily J. Kim, Mi-Sun Kuehn, Hye Sun Metcalfe, Dean D.
Description	Country affiliation: United States Author Affiliation: Kuehn HS ( Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892, USA.)
Abstract	Activated mast cells are a major source of the eicosanoids PGD(2) and leukotriene C(4) (LTC(4)), which contribute to allergic responses. These eicosanoids are produced following the ERK1/2-dependent activation of cytosolic phospholipase A(2), thus liberating arachidonic acid, which is subsequently metabolized by the actions of 5-lipoxygenase and cyclooxygenase to form LTC(4) and PGD(2), respectively. These pathways also generate reactive oxygen species (ROS), which have been proposed to contribute to FcepsilonRI-mediated signaling in mast cells. In this study, we demonstrate that, in addition to ERK1/2-dependent pathways, ERK1/2-independent pathways also regulate FcepsilonRI-mediated eicosanoid and ROS production in mast cells. A role for the Tec kinase Btk in the ERK1/2-independent regulatory pathway was revealed by the significantly attenuated FcepsilonRI-dependent PGD(2), LTC(4), and ROS production in bone marrow-derived mast cells of Btk(-/-) mice. The FcepsilonRI-dependent activation of Btk and eicosanoid and ROS generation in bone marrow-derived mast cells and human mast cells were similarly blocked by the PI3K inhibitors, Wortmannin and LY294002, indicating that Btk-regulated eicosanoid and ROS production occurs downstream of PI3K. In contrast to ERK1/2, the PI3K/Btk pathway does not regulate cytosolic phospholipase A(2) phosphorylation but rather appears to regulate the generation of ROS, LTC(4), and PGD(2) by contributing to the necessary Ca(2+) signal for the production of these molecules. These data demonstrate that strategies to decrease mast cell production of ROS and eicosanoids would have to target both ERK1/2- and PI3K/Btk-dependent pathways.
ISSN	00221767
e-ISSN	15506606
Journal	The Journal of Immunology
Issue Number	11
Volume Number	181
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2008-12-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Antigens Pharmacology Leukotriene C4 Immunology Mast Cells Phosphatidylinositol 3-kinases Prostaglandin D2 Protein-tyrosine Kinases Reactive Oxygen Species Androstadienes Animals Genetics Metabolism Arachidonate 5-lipoxygenase Arachidonic Acid Bone Marrow Cells Enzymology Calcium Signaling Drug Effects Chromones Enzyme Activation Enzyme Inhibitors Hypersensitivity Biosynthesis Map Kinase Signaling System Mice Mice, Knockout Mitogen-activated Protein Kinase 1 Mitogen-activated Protein Kinase 3 Morpholines Antagonists & Inhibitors Phospholipases A2, Cytosolic Phosphorylation Research Support, N.i.h., Intramural Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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