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Roles of MAPK pathway activation during cytokine induction in BEAS-2B cells exposed to fine World Trade Center (WTC) dust.

Authors
Wang-S; Prophete-C; Soukup-JM; Chen-L-C; Costa-M; Ghio-A; Qu-Q; Cohen-MD; Chen-H
Source
J Immunotoxicol 2010 Oct-Dec; 7(4):298-307
NIOSHTIC No.
20039068
Abstract
The World Trade Center (WTC) collapse on September 11, 2001 released copious amounts of particulate matter (PM) into the atmosphere of New York City. Follow-up studies on persons exposed to the dusts have revealed a severely increased rate for asthma and other respiratory illnesses. There have only been a few studies that have sought to discern the possible mechanisms underlying these untoward pathologies. In one study, an increased cytokine release was detected in cells exposed to WTC fine dusts (PM2.5 fraction or WTC2.5). However, the mechanism(s) for these increases has yet to be fully defined. Because activation of the mitogen-activated protein kinase (MAPK) signaling pathways is known to cause cytokine induction, the current study was undertaken to analyze the possible involvement of these pathways in any increased cytokine formation by lung epithelial cells (as BEAS-2B cells) exposed to WTC2.5. Our results showed that exposure to WTC2.5 for 5 hr increased interleukin-6 (IL-6) mRNA expression in BEAS-2B cells, as well as its protein levels in the culture media, in a dose-dependent manner. Besides IL-6, cytokine multiplex analyses revealed that formation of IL-8 and -10 was also elevated by the exposure. Both extracellular signal-regulated kinase (ERK) and p38, but not c-Jun N-terminal protein kinase, signaling pathways were found to be activated in cells exposed to WTC2.5. Inactivation of ERK signaling pathways by PD98059 effectively blocked IL-6, -8, and -10 induction by WTC2.5; the p38 kinase inhibitor SB203580 significantly decreased induction of IL-8 and -10. Together, our data demonstrated activation of MAPK signaling pathway(s) likely played an important role in the WTC2.5-induced formation of several inflammatory (and, subsequently, anti-inflammatory) cytokines. The results are important in that they help to define one mechanism via which the WTC dusts may have acted to cause the documented increases in asthma and other inflammation-associated respiratory dysfunctions in the individuals exposed to the dusts released from the WTC collapse.
Keywords
Particulates; Particulate-dust; Dusts; Dust-particles; Respiratory-system-disorders; Respirable-dust; Bronchial-asthma; Pulmonary-system-disorders; Lung-disorders; Pathology; Proteins; Cytology; Cytopathology; Recombinant-DNA; Dose-response; Immune-reaction; Cell-cultures; Cell-function; Cellular-reactions; Author Keywords: PM2.5; interleukin-6 (IL-6); IL-8; IL-10; ERK; p38
Contact
Haobin Chen, Department of Environmental Medicine, New York University School of Medicine, 57 Old Forge Road, Tuxedo, NY 10987, USA
CODEN
JIOMAP
Publication Date
20101001
Document Type
Journal Article
Email Address
haobin.chen@nyumc.org
Funding Type
Grant
Fiscal Year
2011
NTIS Accession No.
NTIS Price
Identifying No.
Grant-Number-R01-OH-008280
Issue of Publication
4
ISSN
1547-691X
Source Name
Journal of Immunotoxicology
State
NY; NC
Performing Organization
New York University School of Medicine
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