Effects of the inhalation of diesel exhaust, Kanto loam dust, or diesel exhaust without particles on immune responses in mice exposed to Japanese cedar (Cryptomeria japonica) pollen.
To assess the potential enhancement by air-pollutants of immune responses in mice, especially with regard to allergen-specific immunoglobulin E (IgE) antibody production, female BDF(1) mice (60 mice in each group) were exposed to diesel exhaust (particles, 3.24 mg/m(3); nitrogen dioxide, 1.0 ppm: DE group), Kanto loam dust (particles, 3.29 mg/m(3); nitrogen dioxide, 0.01 ppm: KLD group), diesel exhaust without particles (particles, 0.01 mg/m(3); nitrogen dioxide, 1.1 ppm: DEG group), or clean air (pollen and control groups) for 16 h/day, 5 days/wk for 24 wk, as well as to Japanese cedar pollen (JCP) (around 550,000 grains of JCP/m(3)) for 2 days/wk in the same period. The control group was exposed to clean air alone throughout the experiment. The mean values for Japanese cedar pollen allergens (JCPAs)-specific immunoglobulin E (IgE) antibody titers in mice sera measured by enzyme-linked immunosorbent assay (ELISA) in the DE, KLD, and DEG groups were higher than that for the pollen alone group, but not significantly, after both 12 and 24 wk of exposure time. The percentages of animals expressing more than the minimum ELISA titer of JCPAs-specific IgE antibodies in each group were 22% (DE and pollen groups) and 27% (KLD and DEG groups) of the totals at wk 12, and no statistical differences were observed among the groups. However, at wk 24 in the DE, KLD, and DEG groups the responders comprised 73%, 63%, and 67%, respectively, significantly higher than the 33% for the pollen alone group. No significant differences were observed among the DE, KLD, and DEG groups. A slight dose-dependent increase of proliferative responses of mouse cervical lymph node cells to JCPAs in both DE and KLD groups was observed, but not in the DEG group. Remarkable decrease of interferon-gamma and significant increase of interleukin-4 in the nasal lavage fluid were apparent after DE or DEG exposure, but not in the KLD group. These results suggest that these air pollutants (DE, KLD, and DEG) enhance the production of IgE antibodies in mice, with similar adjuvant activities in each case. Furthermore, in the early phase of exposure in which sensitization occurred with exposure to pollen, the fine particles and gas components are considered to have exhibited different enhancing mechanisms in mice as follows: (1) The fine particles augmented production of IgE antibodies through activation of T lymphocytes, and (2) the gas components exhibited almost no action on T lymphocytes, but directly induced disorders of the cytokine network and augmented the production of IgE antibodies.
Maejima
K
K
Energy and Environment Research Division, Japan Automobile Research Institute, 2530 Karima, Tsukuba-shi, Ibaraki 305-0822, Japan. kmae@jari.or.jp
Tamura
K
K
Nakajima
T
T
Taniguchi
Y
Y
Saito
S
S
Takenaka
H
H
D000393:Air Pollutants / Q000009:adverse effects* / Q000276:immunology; D000485:Allergens; D000818:Animals; D000917:Antibody Formation; D028203:Cedrus; D016207:Cytokines / Q000096:biosynthesis* / Q000187:drug effects; D004391:Dust / Q000009:adverse effects*; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D005740:Gases / Q000494:pharmacology; D007073:Immunoglobulin E / Q000096:biosynthesis*; D019570:Inhalation Exposure; D008213:Lymphocyte Activation; D051379:Mice; D010316:Particle Size; D011058:Pollen / Q000009:adverse effects* / Q000276:immunology; D012987:Soil; D013601:T-Lymphocytes / Q000276:immunology; D001335:Vehicle Emissions / Q000009:adverse effects*
D000393:Air Pollutants; D000485:Allergens; D016207:Cytokines; D004391:Dust; D005740:Gases; D012987:Soil; D001335:Vehicle Emissions; D007073:Immunoglobulin E