Abstract
Catecholamines may impact on the pathophysiology of sepsis by attenuating proinflammatory cytokine and augmenting antiinflammatory cytokine production by macrophages. We tested this premise in bone marrow monocyte progenitor-derived macrophages. Polymicrobial sepsis was induced in mice through cecal ligation and puncture. ER-MP 12 monocyte progenitors were isolated and differentiated into macrophages in vitro 72 hr later. Lipopolysaccharide (LPS)-stimulated cytokine production was measured with and without epinephrine, IL-10 and anti-IL-10 antibody. Epinephrine significantly increased IL-10 production, but attenuated TNF-alpha release exclusively through beta2 adrenergic receptors, and is independent of IL-10 production. Together, these results suggest that epinephrine can promote a potent antiinflammatory response in sepsis.
Publication types
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Comparative Study
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Adrenergic beta-Antagonists / pharmacology
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Animals
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Antibodies / pharmacology
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Atenolol / pharmacology
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Bone Marrow / drug effects
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Bone Marrow / metabolism*
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Cell Differentiation / drug effects
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Cytokines / metabolism*
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Disease Models, Animal
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Drug Interactions
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Endotoxins / pharmacology
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Enzyme-Linked Immunosorbent Assay / methods
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Epinephrine / metabolism*
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Epinephrine / pharmacology
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Interleukin-10 / immunology
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Interleukin-10 / metabolism
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Interleukin-10 / pharmacology
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Laparotomy / methods
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Lipopolysaccharides / pharmacology
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Macrophage Activation / drug effects
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Macrophage Activation / physiology
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Macrophages / drug effects
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Macrophages / metabolism*
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Male
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Mice
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Myeloid Progenitor Cells / drug effects
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Myeloid Progenitor Cells / physiology*
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Propanolamines / pharmacology
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Random Allocation
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Sepsis / immunology
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Sepsis / physiopathology*
Substances
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Adrenergic beta-Antagonists
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Antibodies
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Cytokines
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Endotoxins
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Lipopolysaccharides
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Propanolamines
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Interleukin-10
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ICI 118551
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Atenolol
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Epinephrine