Effect of pulsed electromagnetic field treatment on programmed resolution of inflammation pathway markers in human cells in culture
Published online 2015 Feb 23. doi: 10.2147/JIR.S78631
1Nicole Kubat Consulting, Pasadena, CA, USA
2Life Science Department, Regenesis Biomedical, Inc., Scottsdale, AZ, USA
Correspondence: John Moffett, Regenesis Biomedical, Inc., 5301 North Pima Road, Scottsdale, AZ 85250-3773 USA, Tel +1 480 970 4970, Fax +1 866 857 8792, Email moc.oibsiseneger@tteffom
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Inflammation is a complex process involving distinct but overlapping biochemical and molecular events that are highly regulated. Pulsed electromagnetic field (PEMF) therapy is increasingly used to treat pain and edema associated with inflammation following surgery involving soft tissue. However, the molecular and cellular effects of PEMF therapy on pathways involved in the resolution of inflammation are poorly understood. Using cell culture lines relevant to trauma-induced inflammation of the skin (human dermal fibroblasts, human epidermal keratinocytes, and human mononuclear cells), we investigated the effect of PEMF on gene expression involved in the acute and resolution phases of inflammation. We found that PEMF treatment was followed by changes in the relative amount of messenger (m)RNAs encoding enzymes involved in heme catabolism and removal of reactive oxygen species, including an increase in heme oxygenase 1 and superoxide dismutase 3 mRNAs, in all cell types examined 2 hours after PEMF treatment. A relative increase in mRNAs encoding enzymes involved in lipid mediator biosynthesis was also observed, including an increase in arachidonate 12- and 15-lipoxygenase mRNAs in dermal fibroblasts and epidermal keratinocytes, respectively. The relative amount of both of these lipoxygenase mRNAs was elevated in mononuclear cells following PEMF treatment relative to nontreated cells. PEMF treatment was also followed by changes in the mRNA levels of several cytokines. A decrease in the relative amount of interleukin 1 beta mRNA was observed in mononuclear cells, similar to that previously reported for epidermal keratinocytes and dermal fibroblasts. Based on our results, we propose a model in which PEMF therapy may promote chronic inflammation resolution by mediating gene expression changes important for inhibiting and resolving inflammation.
Understanding the cellular and molecular mechanisms of inflammation is important for the development of new therapies to treat important health conditions such as inflammatory pain and chronic inflammation. PEMF is a biophysical therapeutic modality based on the delivery of pulsed electromagnetic fields. Although it has been in use for over several decades for the treatment of inflammation, little is known about its biological mechanism of action. Findings from the current study support previously reported data, suggesting PEMF treatment leads to gene expression changes of the factors involved in regulating inflammation, including inflammation resolution. Based on these results, we hypothesize that PEMF-associated analgesia reported in clinical studies may be due to such gene expression changes. Further studies are warranted to further test this hypothesis and to gain additional insight into the mechanisms of action of this novel analgesic modality.