NDLI: Tricyclic antidepressants prevent the differentiation of monocytes into macrophage-like cells in vitro

Content Provider	Springer Nature Link
Author	Ying, G. Karlsson, H. DePierre, J.W. Nässberger, L.
Copyright Year	2002
Abstract	The investigation was designed to determine whether the two tricyclic antidepressant agents (TCAs) clomipramine and imipramine and the selective reuptake inhibitor citalopram affect differentiation of human monocytes to macrophage-like cells (MAC-LCs). We established primary adherent cultures of peripheral blood monocytes and monitored their morphology, capacity for phagocytosis and antigen expression during transformation to MAC-LCs. As expected, maturation of monocytes to MACs is accompanied by changes in morphology, elevated expression of the antigens CD16 and CD51 and an increase in the percentage of phagocytic cells. Treatment of cells with the TCAs clomipramine (40 μmol/L) or imipramine (100 μmol/L) and with citalopram (100 μmol/L), for 11 days resulted in the following observations: (1) monocytes treated with TCAs never developed the morphology characteristic of the MAC-LCs; (2) TCAs reduced the percentage of phagocytic cells; (3) TCAs had little influence on the expression of CD14, CD16, CD51, and HLA-DR. However, when added after monocyte differentiation into MAC-LCs, citalopram and clomipramine no longer reduced the percentage of phagocytic cells and these effects were not simply due to irreversible cytotoxicity. Thus clomipramine, imipramine, and citalopram inhibit differentiation of human monocytes into MAC-LCs in vitro, but in a reversible manner.
Starting Page	425
Ending Page	437
Page Count	13
File Format	PDF
ISSN	07422091
Journal	Cell Biology and Toxicology
Volume Number	18
Issue Number	6
e-ISSN	15736822
Language	English
Publisher	Kluwer Academic Publishers
Publisher Date	2002-01-01
Publisher Place	Dordrecht
Access Restriction	Subscribed
Subject Keyword	Pharmacology/Toxicology Biochemistry Cell Biology
Content Type	Text
Resource Type	Article
Subject	Cell Biology Health, Toxicology and Mutagenesis Toxicology

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