SULFUR MUSTARD EXPOSURE ENHANCES FC RECEPTOR EXPRESSION ON HUMAN EPIDERMAL-KERATINOCYTES IN CELL-CULTURE - IMPLICATIONS FOR TOXICITY AND MEDICAL COUNTERMEASURES

Citation
Fm. Cowan et al., SULFUR MUSTARD EXPOSURE ENHANCES FC RECEPTOR EXPRESSION ON HUMAN EPIDERMAL-KERATINOCYTES IN CELL-CULTURE - IMPLICATIONS FOR TOXICITY AND MEDICAL COUNTERMEASURES, Cell biology and toxicology, 14(4), 1998, pp. 261-266
Citations number
43
Categorie Soggetti
Cell Biology",Toxicology
Journal title
ISSN journal
07422091
Volume
14
Issue
4
Year of publication
1998
Pages
261 - 266
Database
ISI
SICI code
0742-2091(1998)14:4<261:SMEEFR>2.0.ZU;2-V
Abstract
Sulfur mustard (HD) is a chemical warfare blister agent. The biochemic al basis of HD-induced vesication is unknown, and no antidote currentl y exists. Basal epidermal cells are a major site of HD toxicity in viv o, with inflammation and HD-increased proteolytic activity implicated as factors that contribute to HD pathology. Fc receptors (FcR) bind to the Fc region of antibody to mediate many effector and regulatory fun ctions that can influence inflammatory responses. FcR are found on all types of immune cells and are also expressed on the surface of human keratinocytes. Assay by fluorescent antibodies demonstrated significan tly enhanced CD32 (FcRII) and CD16 (FcRIII) on human epidermal keratin ocyte (HEK) cell cultures at 8 to 24 h after exposure to HD (50, 100 a nd 200 mu mol/L). The enhanced CD32 was time- and concentration-depend ent and agreed well with the time course of increased proteolysis and cutaneous pathology observed during HD vesication. HD-increased FcR on the surface of HEK might be a mechanism of vesication.