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INCREASED IL-8 AND IL-6 EXPRESSION IN HUMAN AIRWAY EPITHELIAL CELLS EXPOSED TO CARBON ULTRAFINE PARTICLES
Citation:
Silbajoris, R, J M. Samet, A. Lenz, AND I. Jaspers. INCREASED IL-8 AND IL-6 EXPRESSION IN HUMAN AIRWAY EPITHELIAL CELLS EXPOSED TO CARBON ULTRAFINE PARTICLES. Presented at Society of Toxicology Meeting, Nashville, TN, March 17-21,2002.
Description:
INCREASED IL-6 AND IL-8 EXPRESSION IN HUMAN AIRWAY EPITHELIAL CELLS EXPOSED TO CARBON ULTRAFINE PARTICLES.
R Silbajoris1, A G Lenz2, I Jaspers3, J M Samet1. 1NHEERL, USEPA, RTP, NC, USA; 2GSF-Institute for Inhalation Biology, Neuherberg, Germany; 3 CEMLB, UNC-CH, Chapel Hill, NC, USA
Ultrafine particles are a potentially toxic constituent of particulate matter (PM) and may contribute to the health effects of ambient PM. Exposure to extracts or components of PM has been shown to evoke inflammatory responses in cultured normal human airway epithelial cells (NHBE). One of these responses is the expression of pro-inflammatory proteins such as IL-6 and IL-8. The aim of the present study was to characterize the effect of ultrafine elemental carbon particle (EC) exposure on IL-6 and IL-8 expression in NHBE. Particles were generated by spark discharge and had a diameter of 75 nm and a surface area of 750 m2/g. Cells were exposed to 0 to 66 ug/ml of EC for 2 to 30 hr and levels of IL-6 and IL-8 mRNA and protein were measured using real-time fluorescent PCR and ELISA, respectively. After 2 hr of exposure to 33 or 66 ug/ml EC, there were minimal increases in IL-6 and IL-8 mRNA when compared to untreated controls. However, a 24 hr exposure to 33 ug/ml EC showed 9-fold and 12-fold increases in IL-6 and IL-8 mRNA, respectively. Doubling the amount of EC to 66 ug/ml resulted in a 10-fold increase in IL-6 mRNA and a 20-fold increase in IL-8 mRNA. To minimize underestimation of IL-6 and IL-8 protein release caused by non-specific protein binding to EC, a pulsed exposure protocol was used. After exposing NHBE to media with 33 or 66 ug/ml EC for 8 hr to initiate mRNA induction, media was changed so that protein release would take place in media without EC. When compared to controls, this regimen resulted in 5-fold elevations in IL-6 and IL-8 release by NHBE that were exposed to EC for 24 hr. These data show that carbon ultrafine particle exposure induces inflammatory mediator expression, suggesting a contributing mechanism for the health effects of ambient PM inhalation. Further studies will be required to identify the mechanism of IL-8 expression induced by exposure to EC. This abstract of a proposed presentation does not necessarily reflect EPA policy.