-Extremely low frequency electromagnetic fields (ELF-EMF) induce cellular changes and modulate signal transduction pathways, and may be beneficial in the treatment of inflammatory diseases. In this paper we studied two inflammatory chemokines, MCP-1 and RANTES produced by human cultured monocytes isolated from peripheral blood, with or withour PHA and in the absence or presence of 50 Hz magnetic field of 1.0 mT for 24 h. The production of MCP-1 and RANTES was determined by ELISA method. Here, we found that ELF-EMF strongly inhibited the production of these chemokines stimulated by PHA, while the control was not affected. Since MCP-1 and RANTES exert chemoattraction for several populations of inflammatory leukocytes, the inhibitory effect of these chemokines could be one of the mechanisms by which ELF-EMF is therapeutic in inflammatory diseases.

Effects of 50 Hz sinusoidal electromagnetic fields on MCP-1 and RANTES generated from activated human macrophages

DI LUZIO, Silvano;FELACO, Mario;BARBACANE, Renato Carmine;GRILLI, Alfredo;CASTELLANI, Maria Luisa;DI GIOACCHINO, Mario;MERLITTI, Daniele;DE LUTIIS, Maria Anna;DI GIULIO, Camillo;CACCHIO, Marisa Adriana;REALE, Marcella
2001-01-01

Abstract

-Extremely low frequency electromagnetic fields (ELF-EMF) induce cellular changes and modulate signal transduction pathways, and may be beneficial in the treatment of inflammatory diseases. In this paper we studied two inflammatory chemokines, MCP-1 and RANTES produced by human cultured monocytes isolated from peripheral blood, with or withour PHA and in the absence or presence of 50 Hz magnetic field of 1.0 mT for 24 h. The production of MCP-1 and RANTES was determined by ELISA method. Here, we found that ELF-EMF strongly inhibited the production of these chemokines stimulated by PHA, while the control was not affected. Since MCP-1 and RANTES exert chemoattraction for several populations of inflammatory leukocytes, the inhibitory effect of these chemokines could be one of the mechanisms by which ELF-EMF is therapeutic in inflammatory diseases.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11564/119585
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