Serotonin and macrophages

At sites of inflammation, macrophages are exposed to mediators released by activated lymphocytes and aggregated platelets. The lymphokine interferony (IFNy) is a well-known activator of macrophages and induces, for example, increased expression of MHC class II on the plasma membrane of macrophages, rendering these cells capable of participating as antigen-presenting cells. Serotonin, which is likely to be present at sites of inflammation, is capable of suppressing the induction of the IFNy-induced class II expression on macrophages. This inhibition is specific and is blocked by 5-HT, receptor antagonists.

Phagocytosis by macrophages is differentially modulated by serotonin. At low concentrations of IFNy, serotonin augments phagocytosis, whereas at high concentrations of IFNy, serotonin suppresses phagocytosis. These effects were blocked by the 5-HT antagonists spiperone, ketanserin, LY53857, mCCP and PAPP. Thus 5-HT could either counteract or augment the stimulatory effects of cytokines, depending on the overall balance of 5-HT and IFNy, or other inflammatory mediators.

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