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Journal of Environmental Pathology, Toxicology and Oncology
CiteScore™: 1.61 IF: 1.15 5-Year IF: 1.4 SNIP: 0.613 SJR: 0.519

ISSN Print: 0731-8898
ISSN Online: 2162-6537

Journal of Environmental Pathology, Toxicology and Oncology

DOI: 10.1615/JEnvironPatholToxicolOncol.v21.i3.80
10 pages

Formaldehyde Enhances Mite Allergen-induced Eosinophilic Inflammation in the Murine Airway

Kaori Sadakane
Department of Health Sciences, Oita University of Nursing and Health Sciences, Oita, Japan
Hirohisa Takano
Research Team for Health Effects of Air Pollutants, National Institute for Environmental Studies, Ibaraki, Japan
Takamichi Ichinose
Department of Health Sciences, Oita University of Nursing and Health Sciences, Oita, Japan
Rie Yanagisawa
Research Team for Health Effects of Air Pollutants, National Institute for Environmental Studies, Ibaraki, Japan
Takayuki Shibamoto
Department of Environmental Toxicology, University of California Davis, Davis, CA 95616

ABSTRACT

Formaldehyde (FA) irritates the skin, eyes, and respiratory system and is considered to be a typical air pollutant. We investigated the effects of FA on the manifestations of airway inflammation caused by a house-dust mite allergen (Der f). ICR mice were exposed to 0.5% FA mist once a week for 4 weeks. The mice were sensitized intraperitoneally with Der f and ALUM prior to FA exposure. After the last FA exposure, they were instilled intratracheally with Der f. The airway inflammation was subsequently examined. The Der f-specific IgG1 and IgE in plasma as well as the asthma-relevant cytokines in the lungs were measured. We found an increase in the plasma IgG1 production of and in the expression of interleukin-5 (IL-S) and regulated on activation, normal Т cell expressed, and presumably secreted (RANTES) in the lungs of mice treated with Der f. The FA exposure enhanced the manifestation of the histopathological changes caused by Der f. This observation corresponded to the enhancement of IL-5 and RANTES production. However, the antigen-specific IgGI antibody did not increase. The IL-4 cytokine level induced by Der f with or without FA was the same as that of the control. IL-2, granulocyte macrophage-colony stimulating factor (GM-CSF), and antigen-specific IgE were not detected. FA exposure enhanced the eosinophilic airway inflammation and the proliferation of goblet cells, which were induced by a mite allergen responsible for the increased local expression of IL-5 and RANTES.