• pulsed electromagnetic field (PEMF)
• macrophage-mediated inflammation
• peripheral neuropathy

The experimental questions regard the capacity of PEMF to reduce inflammation, and to induce a change in phenotype in macrophages, from a pro-inflammatory (M1) to a pro-resolving state (M2). For reproducibility, measurements of the magnetic field, an analytical and a numerical model of the stimulation device are provided and compared to the field distribution obtained by Dr. F. Fontana. THP-1 cells are differentiated to macrophages M0 with 100 ng/ml of PMA for 24 h, M1 macrophages are obtained by stimulating M0 with 1 ug/ml of LPS for 24 h, and M2 by stimulating M0 with 50 ng/ml of IL-4 for 24 h. Control groups are unstimulated M0, M1 and M2; stimulated groups are M0 and M1, which receive PEMF at 0.3 mT, 20 Hz, duty cycle 10% and carrier frequency 13.5 MHz, 3 h/day for 3 days.
Field distribution from the models is in agreement with the experimental data by Dr. Fontana. The difference between the value obtained here and the one by Dr. Fontana is probably due to the different dimension of the probe loop. RT-PCR on TNF-a, IL-1b, IL-8, IL-6, IL-10 and CD206 shows significant decreases in the expression of pro-inflammatory genes between M1 and M1+PEMF and an increase of anti-inflammatory genes between M0 and M0+PEMF. Cytokine quantitation on TNF-a, IL-1b, IL-8, IL-6 and IL-10 confirmed RT-PCR results. The results are coherent with the literature and suggest that PEMF at these parameters will not cause an inflammatory response and could help in reducing chronic inflammatory states.