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Text
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URL Address
<a href="http://doi.org/10.1016/j.jaci.2015.06.030" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.jaci.2015.06.030</a>
Pages
289–298
Issue
1
Volume
137
Dublin Core
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Title
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Leukotriene D4 and prostaglandin E2 signals synergize and potentiate vascular inflammation in a mast cell-dependent manner through cysteinyl leukotriene receptor 1 and E-prostanoid receptor 3.
Publisher
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The Journal of allergy and clinical immunology
Date
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2016
2016-01
Subject
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Animals; c-fos; Capillary Permeability; Cell Line; CysLT(1)R; Dinoprostone/*immunology; E-prostanoid receptor 3; Edema/immunology; EP3 Subtype/*immunology; extracellular signal-regulated kinase; Humans; Inbred BALB C; Inbred C57BL; Inflammation/immunology; leukotriene D(4); Leukotriene D4/*immunology; Leukotriene/*immunology; macrophage inflammatory protein 1beta; Mast cells; Mast Cells/*immunology; Mice; prostaglandin D(2); Prostaglandin E; prostaglandin E(2); protein kinase G; Receptors; Transgenic; Tumor
Creator
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Kondeti Vinay; Al-Azzam Nosayba; Duah Ernest; Thodeti Charles K; Boyce Joshua A; Paruchuri Sailaja
Description
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BACKGROUND: Although arachidonic acid metabolites, cysteinyl leukotrienes (cys-LTs; leukotriene [LT] C4, LTD4, and LTE4), and prostaglandin (PG) E2 are generated at the site of inflammation, it is not known whether crosstalk exists between these 2 classes of inflammatory mediators. OBJECTIVE: We sought to determine the role of LTD4-PGE2 crosstalk in inducing vascular inflammation in vivo, identify effector cells, and ascertain specific receptors and pathways involved in vitro. METHODS: Vascular (ear) inflammation was assessed by injecting agonists into mouse ears, followed by measuring ear thickness and histology, calcium influx with Fura-2, phosphorylation and expression of signaling molecules by means of immunoblotting, PGD2 and macrophage inflammatory protein 1beta generation by using ELISA, and expression of transcripts by using RT-PCR. Candidate receptors and signaling molecules were identified by using antagonists and inhibitors and confirmed by using small interfering RNA. RESULTS: LTD4 plus PGE2 potentiated vascular permeability and edema, gearing the system toward proinflammation in wild-type mice but not in Kit(W-sh) mice. Furthermore, LTD4 plus PGE2, through cysteinyl leukotriene receptor 1 (CysLT1R) and E-prostanoid receptor (EP) 3, enhanced extracellular signal-regulated kinase (Erk) and c-fos phosphorylation, inflammatory gene expression, macrophage inflammatory protein 1beta secretion, COX-2 upregulation, and PGD2 generation in mast cells. Additionally, we uncovered that this synergism is mediated through Gi, protein kinase G, and Erk signaling. LTD4 plus PGE2-potentiated effects are partially sensitive to CysLT1R or EP3 antagonists but completely abolished by simultaneous treatment both in vitro and in vivo. CONCLUSIONS: Our results unravel a unique
Identifier
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<a href="http://doi.org/10.1016/j.jaci.2015.06.030" target="_blank" rel="noreferrer noopener">10.1016/j.jaci.2015.06.030</a>
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Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2016
Al-Azzam Nosayba
Animals
Boyce Joshua A
c-fos
Capillary Permeability
Cell Line
CysLT(1)R
Department of Integrative Medical Sciences
Dinoprostone/*immunology
Duah Ernest
E-prostanoid receptor 3
Edema/immunology
EP3 Subtype/*immunology
extracellular signal-regulated kinase
Humans
Inbred BALB C
Inbred C57BL
Inflammation/immunology
Kondeti Vinay
leukotriene D(4)
Leukotriene D4/*immunology
Leukotriene/*immunology
macrophage inflammatory protein 1beta
Mast cells
Mast Cells/*immunology
Mice
NEOMED College of Medicine
Paruchuri Sailaja
prostaglandin D(2)
Prostaglandin E
prostaglandin E(2)
protein kinase G
Receptors
The Journal of allergy and clinical immunology
Thodeti Charles K
Transgenic
Tumor