title: Extremely low frequency electromagnetic field enhances human keratinocyte cell growth and decreases proinflammatory chemokine production.
abstract: BACKGROUND
  Proliferation and differentiation of keratinocytes are central processes in tissue regeneration after injury. Chemokines, produced by a wide range of cell types including keratinocytes, play a regulatory role in inflammatory skin diseases. Several studies have shown that an electromagnetic field (EMF) can influence both inflammatory processes and repair mechanisms including wound healing on different tissue models.
  
  
  OBJECTIVE
  To elucidate the effect of extremely low frequency EMF (ELF-EMF) on keratinocyte proliferation and production of chemokines [RANTES, monocyte chemoattractant protein (MCP)-1, macrophage inflammatory protein (MIP)-1 alpha and interleukin (IL)-8] in order to evaluate a potential therapeutic use of magnetic fields.
  
  
  METHODS
  The human keratinocyte cell line HaCaT was exposed at 1 mT, 50 Hz for different lengths of time and compared with unexposed control cells. Cell growth and viability were evaluated at different exposure times by cell count and trypan blue exclusion. Chemokine production and expression were analysed by enzyme-linked immunosorbent assay (ELISA) and by real-time polymerase chain reaction. Total NF-kappaB p65 was quantified by ELISA.
  
  
  RESULTS
  Significantly increased growth rates were observed after 48 h of EMF exposure as compared with control cells, while no difference in cell viabilities were detected. Gene expression and release of RANTES, MCP-1, MIP-1 alpha and IL-8 were significantly reduced after 72 h of exposure. NF-kappaB levels became almost undetectable after only 1 h of EMF exposure, and were inversely correlated with cell density.
  
  
  CONCLUSIONS
  Our results show that ELF-EMF modulates chemokine production and keratinocyte growth through inhibition of the NF-kappaB signalling pathway and thus may inhibit inflammatory processes. ELF-EMF could represent an additional therapeutic approach in the treatment of skin injury.
authors.affiliation: Department of Oncology and Neurosciences, University G. d'Annunzio of Chieti-Pescara, 66013 Chieti, Italy.
authors.forename: G
authors.initials: G
authors.lastname: Vianale
authors.forename: M
authors.initials: M
authors.lastname: Reale
authors.forename: P
authors.initials: P
authors.lastname: Amerio
authors.forename: M
authors.initials: M
authors.lastname: Stefanachi
authors.forename: S
authors.initials: S
authors.lastname: Di Luzio
authors.forename: R
authors.initials: R
authors.lastname: Muraro
mesh_terms: D049109:Cell Proliferation / Q000528:radiation effects*; D018946:Chemokine CCL5 / Q000378:metabolism; D018925:Chemokines / Q000378:metabolism* / Q000528:radiation effects; D003872:Dermatitis / Q000532:radiotherapy*; D004307:Dose-Response Relationship, Radiation; D004574:Electromagnetic Fields; D004797:Enzyme-Linked Immunosorbent Assay / Q000379:methods; D015870:Gene Expression; D006801:Humans; D016209:Interleukin-8 / Q000378:metabolism / Q000528:radiation effects; D015603:Keratinocytes / Q000378:metabolism / Q000528:radiation effects*; D016328:NF-kappa B / Q000378:metabolism / Q000528:radiation effects; D020133:Reverse Transcriptase Polymerase Chain Reaction / Q000379:methods; D016896:Treatment Outcome; D014945:Wound Healing
chemical_list: D018946:Chemokine CCL5; D018925:Chemokines; D016209:Interleukin-8; D016328:NF-kappa B