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Formaldehyde exposure induces airway inflammation by increasing eosinophil infiltrations through the regulation of reactive oxygen species production

Authors
Jung, Woon-WonKim, Eun-MiLee, Eun-HeeYun, Hee-JungJu, Hyang-RanJeong, Moon-JinHwang, Kwang-WooSul, DonggeunKang, Hyung-Sik
Issue Date
9월-2007
Publisher
ELSEVIER SCIENCE BV
Keywords
formaldehyde; airway inflammation; eosinophil; reactive oxygen species
Citation
ENVIRONMENTAL TOXICOLOGY AND PHARMACOLOGY, v.24, no.2, pp.174 - 182
Indexed
SCIE
SCOPUS
Journal Title
ENVIRONMENTAL TOXICOLOGY AND PHARMACOLOGY
Volume
24
Number
2
Start Page
174
End Page
182
URI
https://scholar.korea.ac.kr/handle/2021.sw.korea/125728
DOI
10.1016/j.etap.2007.05.001
ISSN
1382-6689
Abstract
Formaldehyde (FA) is a well-known cytotoxic irritant to the airways, but the mechanism of airway inflammation due to EA has not been clarified. In the present study, C57BL/6 mice were exposed to two concentrations (5 and 10 ppm) of FA for 6 h/day, 5 days/week, for 2 weeks. The FA-exposed mice had much higher number of CCR3(+) eosinophils than control mice, and showed upregulated gene expression of CC-chemokine receptor-3 (CCR3), eotaxin and intercellular adhesion molecules-1 (ICAM-1) as well as an increased expression of proinflammatory and Th2 cytokines, such as interleukin (IL)- 1 beta, IL-4 and IL-5. In addition, FA exposure revealed a considerable increase in the serum levels of IgGl, IgG3, IgA and IgE compared to controls. Histopathological analysis of the lung tissues demonstrated eosinophils and mononuclear cell infiltration of the alveolar cell walls and alveolar spaces. Gene expression of thioredoxin (TRX), redox-regulating antioxidant proteins, was markedly suppressed in EA-exposed mice, and thereby intracellular ROS levels were increased along with increased FA concentration. These results were consistent with an increase in the number of CCR3-expressing eosinophils, and indicate that FA-induced ROS was generated from eosinophils recruited to the inflammatory sites of the airways. (c) 2007 Elsevier B.V. All rights reserved.
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