, Volume 15, Issue 9, pp 1147–1164

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

Clearance of dead cells: mechanisms, immune responses and implication in the development of diseases

DOI: 10.1007/s10495-010-0490-z

Cite this article as:
Dini, L. Apoptosis (2010) 15: 1147. doi:10.1007/s10495-010-0490-z


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 [Ca2+]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.


PhagocytosisCigarette smokeStatic magnetic fieldInflammation

Copyright information

© Springer Science+Business Media, LLC 2010

Authors and Affiliations

  1. 1.Department Biological and Environmental Science and Technology (Di.S.Te.B.A.)University of the SalentoLecceItaly