Autocrine actions of macrophage-derived catecholamines on interleukin-1 β

• Published in: Journal of neuroimmunology Vol. 160; no. 1; pp. 87 - 91
• Main Authors: Engler, Kristie L., Rudd, Meghan L., Ryan, John J., Stewart, Jennifer K., Fischer-Stenger, Krista
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier B.V 01.03.2005
• Subjects: Adjuvants, Immunologic - pharmacology; Adrenergic alpha-Antagonists - pharmacology; Adrenergic beta-Antagonists - pharmacology; Animals; Autocrine Communication - drug effects; Autocrine Communication - immunology; Catecholamines; Catecholamines - physiology; Cell Survival - drug effects; Cell Survival - immunology; Extracellular Space - drug effects; Extracellular Space - immunology; Extracellular Space - metabolism; Interleukin-1 - antagonists & inhibitors; Interleukin-1 - biosynthesis; Interleukin-1 - metabolism; Intracellular Fluid - drug effects; Intracellular Fluid - immunology; Intracellular Fluid - metabolism; Lipopolysaccharides - pharmacology; Macrophage Activation - drug effects; Macrophage Activation - immunology; Macrophages; Macrophages, Peritoneal - drug effects; Macrophages, Peritoneal - immunology; Macrophages, Peritoneal - metabolism; Mice; Mice, Inbred CBA; Propanolamines - pharmacology; α-Adrenergic; β-Adrenergic; Catecholamines; β-Adrenergic; Macrophages; α-Adrenergic
• ISSN: 0165-5728; 1872-8421
• DOI: 10.1016/j.jneuroim.2004.11.005

Previous studies indicate that norepinephrine and epinephrine modulate production of interleukin-1 β (IL-1 β) by activated macrophages, but it is not known if macrophage-derived catecholamines affect IL-1 β. In this study, recruited peritoneal macrophages from CBA/J female mice were activated with lipopolysaccharide (LPS) and treated with vehicle or adrenergic receptor antagonists for 24 h. Extracellular and intracellular levels of IL-1 β were measured with ELISA. Treatment with the β-adrenergic receptor antagonists propranolol or ICI 118,551 increased LPS-induced production of IL-1 β, whereas treatment with the α-adrenergic antagonists phentolamine or yohimbine decreased IL-1 β. These findings demonstrate that adrenergic receptor antagonists unmask autocrine actions of macrophage-derived catecholamines on IL-1 β that may influence the inflammatory response.