title: Electromagnetic fields used clinically to improve bone healing also impact lymphocyte proliferation in vitro.
abstract: An important aspect of medical device development is the need to understand how a device produces a specific biological effect. The focus can then be on optimizing that effect by device modification and repeated testing. Several reports from this lab have targeted programmed cell death, or apoptosis, as a cellular pathway that is induced by exposure of transformed leukemic T-cells in culture to specific frequency and intensity electromagnetic fields (EMFs). An EMF delivery device capable of selectively inducing T-cell apoptosis in human tissues could be used to enhance healing by limiting the production of molecules that promote inflammatory disorders such as psoriasis and tendonitis. In the present study, we examined the normal T-cell response to EMF exposure in vitro. In the peripheral blood, 70-80% of the lymphocytes are T-cells, and thus is a rich source of normal cells that match the transformed T-cells used in other experiments (Jurkat cells). We isolated lymphocytes from the peripheral blood of humans and rats, cultured them in nutritive medium and exposed them to either a complex 1.8 mT pulsed EMF (Electrobiology, Inc.), a 0.1 mT, 60 Hz power frequency EMF or a 0.2 mT, 100 Hz sinusoidal EMF. Control lymphocytes were cultured similarly, without field exposure. Lymphocytes were then treated with T-cell mitogens and evaluated for proliferative capacity after an additional 72 hours culture. Results indicate that T-cell proliferation is modulated by in vitro exposure to defined EMFs. The potential use of an EMF delivery device capable of selectively inducing such T-cell effects is discussed.
authors.affiliation: Terre Haute Center for Medical Education, Indiana University School of Medicine, Terre Haute, IN 47809, USA.
authors.forename: M T
authors.initials: MT
authors.lastname: Johnson
authors.forename: A
authors.initials: A
authors.lastname: Vanscoy-Cornett
authors.forename: D N
authors.initials: DN
authors.lastname: Vesper
authors.forename: J A
authors.initials: JA
authors.lastname: Swez
authors.forename: J K
authors.initials: JK
authors.lastname: Chamberlain
authors.forename: M B
authors.initials: MB
authors.lastname: Seaward
authors.forename: G
authors.initials: G
authors.lastname: Nindl
mesh_terms: D000818:Animals; D002455:Cell Division; D002478:Cells, Cultured; D004247:DNA / Q000096:biosynthesis; D004574:Electromagnetic Fields; D017102:Fracture Healing; D006801:Humans; D008213:Lymphocyte Activation; D051381:Rats; D017207:Rats, Sprague-Dawley; D013601:T-Lymphocytes / Q000502:physiology
chemical_list: D004247:DNA