Pulsed electromagnetic fields decrease proinflammatory cytokine secretion (IL-1β and TNF-α) on human fibroblast-like cell culture

Abstract

The clinical use of pulsed electromagnetic fields (PEMF) in osteoarticular pathology is widely extended, although the mechanisms involved are unknown. The aim of this study was to evaluate the action of a new protocol of treatment with PEMF on liquid medium cultures of fibroblast-like cells derivates of mononuclear peripheral blood cells. Fibroblast-like cells growth was obtained in liquid medium culture from mononuclear cells (MNC) of human peripheral blood. The PEMF irradiation protocol included an intensity of 2.25 mT, a frequency of 50 Hz and an application time of 15 min on days 7, 8 and 9 of cell culture. Immunophenotype was performed with specific heterologous monoclonal antibodies for each cell receptor (Vimentin, Cytokeratin, CD34, CD41, CD61 and CD68). The cytokines' production was determined in the supernatant of the culture medium by means of the Luminex technology. The immunophenotype did not show any statistical difference on comparing treated against non-treated cell cultures on any of the days. In the treatment cell population, the proinflammatory cytokines, IL-1β and TNF-α showed a significant decrease on days 14 and 21 of the culture, whilst IL-10 increased significantly on day 21. It is concluded that PEMF irradiation does not alter the cell immunophenotype of the fibroblast-like cell population, but does provoke a decrease in the production of inflammatory-type cytokines (IL-1β, TNF-α) and an increase in cytokines of lymphocytic origin (IL-10). These facts coincide with the chronology of the clinical effect undergone by patients with osteoarticular pathology after PEMF irradiation.

Electromagnetic fields (EMFs) and adenosine receptors modulate prostaglandin E2 and cytokine release in human osteoarthritic synovial fibroblasts

“…To our knowledge, very few studies have investigated the EMF effect on SFs and no data have been reported on human OASFs and the modulation of cytokine release (Murray et al, 1988; Marino et al, 2003; Varani et al, 2008; De Mattei et al, 2009). On the other hand, our data agree with previous studies showing that EMFs inhibit PGE 2 and cytokine production both in “in vitro” and in “in vivo” models, as well as in clinical studies (Lohmann et al, 2000; Chang et al, 2005; Benazzo et al, 2008a; De Mattei et al, 2009; Gomez‐Ochoa et al, 2010; Rohde et al, 2010). Here we show for the first time that EMFs significantly modulate the release of PGE 2 and both inflammatory and anti‐inflammatory cytokines in human OASFs, suggesting that cytokine production may be one of the most important functions affected by EMFs in these cells.…”

Treatment by Therapeutic Magnetic Resonance (TMR™) increases fibroblastic activity and keratinocyte differentiation in anin vitromodel of 3D artificial skin

“…Recently, several reports have evaluated the effects of extremely low‐frequency electromagnetic fields (EMFs) on tissue repair (Pesce et al ., ). In particular, the data support an anti‐inflammatory effect of EMFs by modulating cytokine profiles that drive the transition from a chronic pro‐inflammatory state of the healing process to an anti‐inflammatory state (Gomez‐Ochoa et al ., ). Molecular clarification of the mechanisms involved in the modulation of inflammatory factors following exposure to EMFs will provide a better understanding of the cellular responses induced by EMFs and provide a potential, additional treatment in non‐responding, chronic wounds (Lin et al , ).…”

Extremely low frequency electromagnetic field and wound healing: implication of cytokines as biological mediators

“…These results are in accordance with early mediated reduction of NF-kB levels by EMFs described by Vianale et al on keratinocytes. Similarly, a recent study concluded that PEMF irradiation, not altering the cell immune-phenotype of the fibroblastlike cell population, provokes a decrease in the production of inflammatory-type cytokines (IL-1␤, TNF-␣) and an increase in cytokines of lymphocytic origin (IL-10) [119].…”