Prostaglandin E2 inhibits TNF production in murine bone marrow-derived dendritic cells

Exposure to pathogens induces dendritic cells to release inflammatory cytokines and chemokines. The inflammatory response is controlled by endogenous agents such as anti-inflammatory cytokines, glucocorticoids, anti-inflammatory neuropeptides, and lipid mediators. This study is the first report on t...

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Bibliographic Details
Published in:Cellular immunology 2003-06, Vol.223 (2), p.120-132
Main Authors: Vassiliou, Evros, Jing, Huie, Ganea, Doina
Format: Article
Language:English
Subjects:
Animals
Anti-Inflammatory Agents - pharmacology
Bone Marrow Cells - drug effects
Bone Marrow Cells - metabolism
CD11c Antigen - metabolism
Dendritic cells
Dendritic Cells - drug effects
Dendritic Cells - metabolism
Dinoprostone - administration & dosage
Dinoprostone - pharmacology
Enzyme-Linked Immunosorbent Assay
EP2/EP4 receptors
Flow Cytometry
Inflammation
Injections, Intraperitoneal
Lipopolysaccharides - administration & dosage
Lipopolysaccharides - pharmacology
Male
Mice
PGE2
Receptors, Prostaglandin E - metabolism
Receptors, Prostaglandin E, EP2 Subtype
Receptors, Prostaglandin E, EP4 Subtype
Reverse Transcriptase Polymerase Chain Reaction
TNF
Tumor Necrosis Factor-alpha - analysis
Tumor Necrosis Factor-alpha - biosynthesis
Tumor Necrosis Factor-alpha - drug effects
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Summary:Exposure to pathogens induces dendritic cells to release inflammatory cytokines and chemokines. The inflammatory response is controlled by endogenous agents such as anti-inflammatory cytokines, glucocorticoids, anti-inflammatory neuropeptides, and lipid mediators. This study is the first report on the inhibition by prostaglandin E2 (PGE2) of TNF release from bone marrow-derived dendritic cells stimulated with lipopolysaccharide (LPS), a TLR4 ligand, or peptidoglycan, a TLR2 ligand. The inhibition of TNF occurs at both mRNA and protein level. The inhibitory effect of PGE2 is mediated by the EP2 and EP4 receptors, and involves both PKA signaling and mediation by DC-derived IL-10. Intraperitoneal administration of PGE2 together with LPS results in a reduction in serum TNF and intracellular TNF in peritoneal exudate cells, compared to LPS alone. In addition, administration of PGE2 in vivo reduces the numbers of CD11c+ DCc that accumulate in the peritoneal cavity in response to LPS. The various implications of the PGE2-induced reduction in TNF are discussed.
ISSN:0008-8749
1090-2163
DOI:10.1016/S0008-8749(03)00158-8