Article date: May 2003
By: M Freire‐Garabal, M J Núñez, J Balboa, P López‐Delgado, R Gallego, T García‐Caballero, M D Fernández‐Roel, J Brenlla, M Rey‐Méndez in Volume 139, Issue 2, pages 457-463
In this study, we investigated whether serotonin could regulate the in vitro activity of phagocytosis through 5‐hydroxytryptamine or serotonin (5‐HT1A) receptors.
Mouse peritoneal macrophages were cultured with serotonin and the activity of phagocytosis was assessed by the uptake of zymosan and latex particles added to the culture media. Specific binding of [3H]8‐OH‐DPAT and immunohistochemistry using an affinity‐purified anti‐5‐HT1A‐receptor antibody were assayed in the macrophages. In addition, we took advantage of the availability of pharmacological inhibitors of nuclear factor‐κB (NF‐κB) to explore its role in the regulation of the 5‐HT1A receptor.
Serotonin increased the in vitro activity of phagocytosis in a dose‐dependent manner. The 5‐HT1A receptor agonist (±)‐8‐hydroxy‐2‐(di‐n‐propyl‐amino)‐tetralin (R(+)‐8‐OH‐DPAT) reproduced these effects. Serotonin‐ or R(+)‐8‐OH‐DPAT‐induced increases in phagocytosis were blocked by the 5‐HT1A receptor antagonist WAY100635 and the NF‐κB inhibitor pyrrolidinedithiocarbamate. Moreover, mouse peritoneal macrophages expressed specific binding sites for [3H]8‐OH‐DPAT when cultivated in the presence of zymosan or latex beads. Immunohistochemistry confirmed the expression of the 5‐HT1A receptor protein in the macrophages.
These results show that serotonin can upregulate the activity of peritoneal macrophages through 5‐HT1A receptors.
In this study, we investigated whether serotonin could regulate the in vitro activity of phagocytosis through 5‐hydroxytryptamine or serotonin (5‐HT1A) receptors.
Mouse peritoneal macrophages were cultured with serotonin and the activity of phagocytosis was assessed by the uptake of zymosan and latex particles added to the culture media. Specific binding of [3H]8‐OH‐DPAT and immunohistochemistry using an affinity‐purified anti‐5‐HT1A‐receptor antibody were assayed in the macrophages. In addition, we took advantage of the availability of pharmacological inhibitors of nuclear factor‐κB (NF‐κB) to explore its role in the regulation of the 5‐HT1A receptor.
Serotonin increased the in vitro activity of phagocytosis in a dose‐dependent manner. The 5‐HT1A receptor agonist (±)‐8‐hydroxy‐2‐(di‐n‐propyl‐amino)‐tetralin (R(+)‐8‐OH‐DPAT) reproduced these effects. Serotonin‐ or R(+)‐8‐OH‐DPAT‐induced increases in phagocytosis were blocked by the 5‐HT1A receptor antagonist WAY100635 and the NF‐κB inhibitor pyrrolidinedithiocarbamate. Moreover, mouse peritoneal macrophages expressed specific binding sites for [3H]8‐OH‐DPAT when cultivated in the presence of zymosan or latex beads. Immunohistochemistry confirmed the expression of the 5‐HT1A receptor protein in the macrophages.
These results show that serotonin can upregulate the activity of peritoneal macrophages through 5‐HT1A receptors.
British Journal of Pharmacology (2003) 139, 457–463. doi:10.1038/sj.bjp.0705188
DOI: 10.1038/sj.bjp.0705188
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