ISSN:
1600-079X
Source:
Blackwell Publishing Journal Backfiles 1879-2005
Topics:
Medicine
Notes:
Abstract: The pineal hormone melatonin, due to its lipophilic nature, has access to every cell and every part of a cell in the body, suggesting that it could exert effects on blood immune cells. The regulation of the activation of monocytes may be important in a number of diseases, especially pathophysiological conditions associated with inflammatory reactions. Considering this, a study on the effect of melatonin on monocytes in whole blood was carried out. Melatonin added at a final concentration of 5 ng/mL to whole blood in vitro reduced lipopolysaccharide (LPS)-induced tissue factor (TF) activity in monocytes by 55% in blood from a group of subjects with melatonin-sensitive cells. At even lower concentrations of melatonin (20-50 pg/mL) and in the physiological range, a trend of suppressed LPS-induced TF activity by ∼ 20% was seen. A further indication of a downregulation of LPS-stimulated monocytes by melatonin was shown by its reduction of LPS-induced tumor necrosis factor (TNF). Twenty to one hundred pg/mL melatonin caused a significant reduction of LPS-induced TNF production by ∼ 25–30%. In contrast, melatonin at a final concentration of 10 pg/mL, added to whole blood incubated with LPS and also the phorbol ester, PMA, caused a signficant rise of 25%; whereas 100 pg/mL enhanced LPS + PMA-induced TNF by ∼ 80% as compared to LPS + PMA alone. These effects were not detectable during the winter darkness of Tromsø (70°N), probably due to the high content of melatonin in the blood even at daytime. These results show that melatonin may have a beneficial effect by suppressing the expression of TF activity in LPS-stimulated monocytes. Furthermore, the results indicate that LPS-induced TF in monocytes of whole blood is independent of protein kinase C (PKC) activation. Melatonin is probably amplifying cellular activation reactions that are PKC-dependent. This may be physiologically important in upregulation of the immune system.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1111/j.1600-079X.1999.tb00566.x
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