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ULTRAFINE CARBON PARTICLES INDUCE IL-8 EXPRESSION IN HUMAN AIRWAY EPITHELIAL CELLS THROUGH A POST-TRANSCRIPTIONAL MECHANISM
Citation:
Samet, J M., W. Reed, A. Lenz, AND Y. M. Kim. ULTRAFINE CARBON PARTICLES INDUCE IL-8 EXPRESSION IN HUMAN AIRWAY EPITHELIAL CELLS THROUGH A POST-TRANSCRIPTIONAL MECHANISM. Presented at American Thoracic Society, Orlando, FL, May 21-26, 2004.
Description:
Ultrafine carbon particles induce IL-8 expression in human airway
epithelial cells through a post-transcritpional mechanism
Epidemiological studies suggest that ultrafine particles contribute to
particulate matter (PM) - induced adverse health effects. IL-8 is an
important pro-inflammatory cytokine in the human lung that is induced in
respiratory cells exposed to a variety of environmental insults, including
ambient air ultrafine particles. In this study, we examined the effect of
a model ultrafine particle on IL-8 expression and the cellular mechanisms
responsible for this event. Here, we report that carbonaceous ultrafine
particles consisting of synthetic elemental carbon particles (UfCP)
markedly increase the expression of interleukin (IL)-8 mRNA and protein,
in normal human bronchial epithelial (NHBE) cells. IL-8 promoter activity
was increased by UfCP exposure in NHBE cells, indicating UfCP-induced IL-8
expression is transcriptionally regulated. IL-8 expression in NHBE is
known to be regulated by NF- B activation. However, UfCP did not induce
I B? degradation, NF- B-DNA binding or NF- B dependent promoter activity
in NHBE cells, indicating that UfCP induces IL-8 expression through a
mechanism that is independent of NF- B activation. Additionally, we
observed that UfCP exposure induces the phosphorylation and activation of
p38 MAPK in a biphasic manner, and that the inhibition of p38 MAPK
activity can block IL-8 mRNA expression induced by UfCP in NHBE cells.
These results demonstrate that UfCP-induces expression of IL-8 involves a
transcriptional mechanism and activation of p38 MAPK in NHBE cells.
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