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Effect of stress-related hormones on macrophage receptors and response to tumor necrosis factor.
|Title||Effect of stress-related hormones on macrophage receptors and response to tumor necrosis factor.|
|Publication Type||Journal Article|
|Year of Publication||1990|
|Authors||Bermudez LE, Wu M, Young LS|
|Date Published||1990 Summer|
|Keywords||Adrenocorticotropic Hormone, Angiotensin II, Corticotropin-Releasing Hormone, Down-Regulation, Epinephrine, Glucagon, Humans, Insulin, Lipopolysaccharides, Luteinizing Hormone, Macrophage Activation, Macrophages, Mycobacterium avium Complex, Mycobacterium avium-intracellulare Infection, Receptors, Cell Surface, Receptors, Tumor Necrosis Factor, Somatostatin, Thyrotropin, Tumor Necrosis Factor-alpha|
Tumor Necrosis Factor (TNF) has been implicated in the early metabolic events following acute tissue injury or sepsis; it increases blood levels of glucocorticoids and glucagon or the cellular responses to the hormones. To examine whether stress-related hormones have any effect on macrophage activation by TNF, human monocyte-derived macrophages were exposed to somatostatin (S), ACTH, angiotensin (An), insulin (I), epinephrine (E), and glucagon (G) at physiologic concentrations. 125I-TNF binding as well as the ability of TNF to activate macrophages to kill an intracellular pathogen (Mycobacterium avium) were measured. While treatment with recombinant interferon gamma increased the number of TNF receptors by 53 +/- 8%, E, I, G, S, ACTH and An decreased the number of receptors by 81 +/- 6%, 83 +/- 6%, 15 +/- 5%, 83 +/- 4%, 17 +/- 4% and 21 +/- 4%, respectively. Treatment with I, E, and S also decreased the ability of macrophages to kill M. avium by 30 +/- 1%, 20 +/- 6%, and 51 +/- 2%, respectively. These in vitro results suggest that stress hormones influence TNF-mediated activation of macrophages.
|Alternate Journal||Lymphokine Res.|