TY - JOUR
T1 - Formaldehyde exposure induces airway inflammation by increasing eosinophil infiltrations through the regulation of reactive oxygen species production
AU - Jung, Woon Won
AU - Kim, Eun Mi
AU - Lee, Eun Hee
AU - Yun, Hee Jung
AU - Ju, Hyang Ran
AU - Jeong, Moon Jin
AU - Hwang, Kwang Woo
AU - Sul, Donggeun
AU - Kang, Hyung Sik
N1 - Funding Information:
This work was supported by a grant of the Ministry of Environment as “The Eco-Technopia 21 project” and by the National R&D Program for Cancer Control, Ministry of Health & Welfare, Republic of Korea (0420160-1).
PY - 2007/9
Y1 - 2007/9
N2 - Formaldehyde (FA) is a well-known cytotoxic irritant to the airways, but the mechanism of airway inflammation due to FA 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)-1β, IL-4 and IL-5. In addition, FA exposure revealed a considerable increase in the serum levels of IgG1, 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 FA-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.
AB - Formaldehyde (FA) is a well-known cytotoxic irritant to the airways, but the mechanism of airway inflammation due to FA 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)-1β, IL-4 and IL-5. In addition, FA exposure revealed a considerable increase in the serum levels of IgG1, 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 FA-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.
KW - Airway inflammation
KW - Eosinophil
KW - Formaldehyde
KW - Reactive oxygen species
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U2 - 10.1016/j.etap.2007.05.001
DO - 10.1016/j.etap.2007.05.001
M3 - Article
C2 - 21783807
AN - SCOPUS:34547104389
SN - 1382-6689
VL - 24
SP - 174
EP - 182
JO - Environmental Toxicology and Pharmacology
JF - Environmental Toxicology and Pharmacology
IS - 2
ER -