Premium
Inorganic arsenite inhibits IgE receptor‐mediated degranulation of mast cells
Author(s) -
Hutchinson Lee M.,
Trinh Benett M.,
Palmer Rachel K.,
Preziosi Christopher A.,
Pelletier Jonathan H.,
Nelson Hannah M.,
Gosse Julie A.
Publication year - 2011
Publication title -
journal of applied toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.784
H-Index - 87
eISSN - 1099-1263
pISSN - 0260-437X
DOI - 10.1002/jat.1585
Subject(s) - degranulation , immunoglobulin e , immunology , mast (botany) , chemistry , receptor , mast cell , medicine , antibody , biochemistry
Millions of people worldwide are exposed to arsenic (As), a toxicant which increases the risk of various cancers, cardiovascular disease and several other health problems. Arsenic is a potent endocrine disruptor, including of the estrogen receptor. It was recently shown that environmental estrogen‐receptor disruptors can affect the signaling of mast cells, which are important players in parasite defense, asthma and allergy. Antigen (Ag) or allergen crosslinking of IgE‐bound receptors on mast cells leads to signaling, culminating in degranulation, the release of histamine and other mediators. Because As is an endocrine disruptor and because endocrine disruptors have been found to affect degranulation, here we have tested whether sodium arsenite affects degranulation. Using the rat basophilic leukemia (RBL) mast cell model, we have measured degranulation in a fluorescence assay. Arsenic alone had no effect on basal levels of degranulation. However, As strongly inhibited Ag‐stimulated degranulation at environmentally relevant concentrations, in a manner that is very dependent on concentrations of both As and Ag. The concentrations of As effective at inhibiting degranulation were not cytotoxic. This inhibition may be a mechanism underlying the traditional Chinese medicinal use of As to treat asthma. These data indicate that As may inhibit the ability of humans to fight off parasitic disease. Copyright © 2010 John Wiley & Sons, Ltd.