Phagocytosis of dying cells: influence of smoking and static magnetic fields

Abstract

It is becoming evident that failure in the removal of dying cells causes and/or promotes the onset of chronic diseases. Impairment of phagocytosis of apoptotic cells can be due not only to genetic or molecular malfunctioning but also to external/environmental factors. Two of these environmental factors have been recently reported to down regulate the clearance of apoptotic cells: cigarette smoke and static magnetic fields. Cigarette smoke contains highly reactive carbonyls that modify proteins which directly/indirectly affects cellular function. Human macrophages interacting with carbonyl or cigarette smoke modified extracellular matrix (ECM) proteins dramatically down regulated their ability to phagocytose apoptotic neutrophils. It was postulated that changes in the ECM environment as a result of cigarette smoke affect the ability of macrophages to remove apoptotic cells. This decreased phagocytic activity was as a result of sequestration of receptors involved in the uptake of apoptotic cells towards that of recognition of carbonyl adducts on the modified ECM proteins leading to increased macrophage adhesion. Downregulation of the phagocytosis of apoptotic cells was also described when performed in presence of static magnetic fields (SMFs) of moderate intensity. SMFs have been reported to perturb distribution of membrane proteins and glycoproteins, receptors, cytoskeleton and trans-membrane fluxes of different ions, especially calcium [Ca(2+)]i, that in turn, interfere with many different physiological activities, including phagocytosis. The effects of cigarette smoke and SMF on the phagocytosis of dying cells will be here discussed.

Inhibition of STAT3- and MAPK-dependent PGE2 synthesis ameliorates phagocytosis of fibrillar β-amyloid peptide (1-42) via EP2 receptor in EMF-stimulated N9 microglial cells

“…Similarly, in this study, we observed an inversed correlation of pro-inflammatory COX-2 and prostaglandin expression with attenuated phagocytosis of 647-fAβ 42 in EMF-stimulated N9 cells. In support of this, down-regulated phagocytosis of latex particles or apoptotic cells has also been observed in other members of the mononuclear phagocyte system, such as macrophages and monocytes, in the presence of static magnetic fields (SMFs) [42–44]. These decreased phagocytic activities were concomitant for driving the expressions of molecular components of various signaling pathways and effector functions, especially intracellular free Ca 2+ ([Ca 2+ ] i ), in the presence of SMFs [42, 44].…”

Does static magnetic field-exposure induced oxidative stress and apoptosis in rat kidney and muscle? Effect of vitamin E and selenium supplementations

“…Based on advanced studies of SMF effects on oxidative stress reactions, the potentially hazardous effect of SMF on living organisms is that exposure to SMF can increase the activity, concentration, and life time of paramagnetic free radicals, which might cause oxidative stress, genetic mutation, and/or apoptosis (Mohtat et al 1998;Zhang et al 2003;Okano 2008;Dini 2010).…”

The Effects of Static Magnetic Field on Rats Brain, Lungs, Liver, Pancreas and Blood Electrolytes

“…Damage to lymphocytes by SMF (7 mT) increased up to 20% when they were treated with ferrous chloride (FeCl2) (Zmyslony et al, 2000;Junji, 2006). Moreover, exposure to SMF could increase the activity, concentration and lifetime of paramagnetic free radicals, leading to oxidative stress, genetic mutation and apoptosis (Zhao, 2011;Dini, 2010), and exposure to SMF initiates an ironmediated process that increases free radical formation in brain cells, leading to the breaking of DNA strands and cell death (Soumaya et al, 2013).…”