Loading…

Environmental pollutant tributyltin promotes Th2 polarization and exacerbates airway inflammation

It has been shown that a relatively high dose of tributyltin (TBT), which is recognized as a particularly notable environmental pollutant, exerts immunotoxic effects such as thymic atrophy viainduction of T cell apoptosis. However, the effect of low doses of TBT on the immune responses remains unkno...

Full description

Saved in:
Bibliographic Details
Published in:European journal of immunology 2004-05, Vol.34 (5), p.1312-1321
Main Authors: Kato, Takuma, Uchikawa, Ryuichi, Yamada, Minoru, Arizono, Naoki, Oikawa, Saeko, Kawanishi, Shosuke, Nishio, Akiyoshi, Nakase, Hiroshi, Kuribayashi, Kagemasa
Format: Article
Language:English
Subjects:
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:It has been shown that a relatively high dose of tributyltin (TBT), which is recognized as a particularly notable environmental pollutant, exerts immunotoxic effects such as thymic atrophy viainduction of T cell apoptosis. However, the effect of low doses of TBT on the immune responses remains unknown. Here we show that environmentally relevant doses of TBT promoted strong Th2 polarization via suppression and augmentation of Th1 and Th2 development, respectively, from naive CD4+ T cells primed with anti‐CD3 and splenic antigen‐presenting cells (APC). TBT‐induced Th2 polarization was indirect, working through APC via suppression of IL‐12 production by macrophages/DC and the augmentation of IL‐10 production by B cells. Th2 polarization was also induced in mice treatedwith TBT and immunized with OVA or infected with Nippostrongylus brasiliensis. Furthermore, airway inflammation in mice sensitized and challenged with OVA was exacerbated by the administration of TBT with concomitant augmentation of Th2‐type immunity. Our results highlight the fact that an important environmental pollutant TBT may present significant risk for the induction of allergic diseases via promotion of Th2 polarization.
ISSN:0014-2980
1521-4141
DOI:10.1002/eji.200324667