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HERO ID
3859092
Reference Type
Journal Article
Title
Diisononyl phthalate induces asthma via modulation of Th1/Th2 equilibrium
Author(s)
Hwang, YH; Paik, MJ; Yee, ST
Year
2017
Is Peer Reviewed?
1
Journal
Toxicology Letters
ISSN:
0378-4274
EISSN:
1879-3169
Publisher
ELSEVIER IRELAND LTD
Location
CLARE
Volume
272
Page Numbers
49-59
Language
English
PMID
28300662
DOI
10.1016/j.toxlet.2017.03.014
Web of Science Id
WOS:000400436400005
URL
https://linkinghub.elsevier.com/retrieve/pii/S037842741730108X
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Abstract
Diisononyl phthalate (DINP), a member of the phthalate family, is used to plasticize polyvinyl chloride (PVC). This chemical is known to enhance airway inflammation in the OVA-induced asthma model (adjuvant effects) and aggravate allergic dermatitis. Moreover, DINP enhances the production of interleukin-4 in activated CD4(+) T cells. However, the effect of DINP itself on the differentiation of naïve CD4(+) T cells into T helper cells (Th1/Th2) in vitro and allergic asthma in vivo has not yet been studied. In this study, DINP was shown to suppress the polarization of Th1 and enhance the polarization of Th2 from naïve CD4(+) T cells in vitro. Also, DINP induced allergic asthma via the production of IL-4, IL-5, IgE and IgG1 and the reduction of IFN-γ and IgG2a. Finally, we confirmed that exposure to DINP induces the infiltration of inflammatory cells and PAS positive cells and increases the expression of caspase-1 and caspase-3 in asthmatic mice. In conclusion, we suggest that DINP as an environmental pollutant or endocrine disruptor (ECD) induces asthma via the modulation of the Th1/Th2 equilibrium and production of Th2 mediated cytokines and immunoglobulin.
Keywords
asthma; airway hyperresonsiveness (AHR); helper T cells (Th cells); diisononyl phthalate (DINP); endocrine disruptor (ECD); environmental pollutant
Tags
IRIS
•
Diisononyl Phthalate (DINP)
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