Abstract
Innate immune cells react to electromagnetic fields (EMF) by generating reactive oxygen species (ROS), crucial intracellular messengers. Discrepancies in applied parameters of EMF studies, e.g., flux densities, complicate direct comparison of downstream anti-oxidative responses and immune regulatory signaling. We therefore compared the impact of different EMF flux densities in human leukemic THP1 cells and peripheral blood mononuclear cells (PBMC) of healthy donors to additionally consider a potential disparate receptivity based on medical origin. ROS levels increased in THP1 cells stimulated with lipopolysaccharide (LPS) after one hour of EMF exposure. Moreover, weak EMF mitigated the depletion of the reducing agent NAD(P)H in THP1. Neither of these effects occurred in PBMC. Landscaping transcriptional responses to varied EMF revealed elevation of the anti-oxidative enzymes PRDX6 (2-fold) and DHCR24 (6-fold) in THP1, implying involvement in lipid metabolism. Furthermore, our study confirmed anti-inflammatory effects of EMF by 6-fold increased expression of IL10. Strikingly, THP1 responded to weak EMF, while PBMC were primarily affected by strong EMF, yet with severe cellular stress and enhanced rates of apoptosis, indicated by HSP70 and caspase 3 (CASP3). Taken together, our results emphasize an altered susceptibility of immune cells of different origin and associate EMF-related effects with anti-inflammatory signaling and lipid metabolism.
Highlights
Reports on the sensitivity of human health to electromagnetic fields (EMF) have accumulated around the globe and manifest clinically as electromagnetic hypersensitivity (EHS) with broad-spectrum symptoms in multiple organs [1,2,3]
Pinpointing the molecular causality for symptoms accounted to EHS to be caused by EMF is complicated by the complex human system responding to the fluctuating factors of the modern environment that it is exposed to on a daily basis, such as infections, medication and psychological factors like stress, and the wide range of frequencies and field strengths emitted from different devices [11]
It was highly interesting that among genes typical for the degradation and regulation of reactive oxygen species (ROS), such as glutathione peroxidases (GPX, [38]; GPX1 and GPX5 elevated in THP1) or oxidation resistance 1 (OXR1, [39]; elevated in peripheral blood mononuclear cells (PBMC)), we found expression levels of genes relevant in the lipid metabolism such as apolipoprotein
Summary
Reports on the sensitivity of human health to electromagnetic fields (EMF) have accumulated around the globe and manifest clinically as electromagnetic hypersensitivity (EHS) with broad-spectrum symptoms in multiple organs [1,2,3]. To WPR, medically preconditioned individuals were suggested to be more susceptible to EHS as their survival rate was found to decrease under EMF exposure [6]. Pinpointing the molecular causality for symptoms accounted to EHS to be caused by EMF is complicated by the complex human system responding to the fluctuating factors of the modern environment that it is exposed to on a daily basis, such as (viral) infections, medication and psychological factors like stress, and the wide range of frequencies and field strengths emitted from different devices (e.g., smartphones, TV, WiFi, radio) [11]. Disparities in exposure conditions, i.e., field strength, are present in in vitro studies focused on EMF-induced effects, which renders direct comparison difficult.
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