title: Investigation of the chemical-induced selective type II (T(H)2) allergic response in mice: effect of the length of the sensitizing phase.
abstract: Allergies are immune system disorders characterized by abnormal, acquired sensitivity to various environmental chemicals. We investigated the mechanism of chemical-induced selective type II (T(H)2) allergy by using three different sensitization protocols and the well-known respiratory sensitizer trimellitic anhydride (TMA). Mice were sensitized for either 1, 2, or 3 weeks. For each sensitization schedule, the mice were allocated into 3 or 4 groups: -/- group, both sensitized and challenged with vehicle; -/+ group, sensitized with vehicle and challenged with 0.1% TMA; +/- group, sensitized with 1% TMA and challenged with vehicle; and +/+ group, both sensitized and challenged with 0.1% TMA. After challenge, we assayed the auricular lymph nodes of all mice for number of lymphocytes, surface antigen expression of B-cells, and local cytokine production, and we measured TMA-specific serum IgE levels. Some parameters in mice sensitized for 1 or 2 wk showed, at most, mild changes. In contrast, all parameters in animals receiving 3-wk sensitization showed marked increases, as well as marked increases in the IgE/major histocompatibility complex (MHC) Class II-positive B-cell population and T(H)2 cell production of IL-10 and IL-13. These results indicate that 3 wk of sensitization according to our protocol led to overt respiratory allergic reactions. While these studies showed that using the approach here, positive reactions were elicited using a typical allergen; whether the same events occur after sensitization by other chemicals that are found in the environment remains uncertain. These findings here should be regarded moreover as preliminary in scope and that additional studies with irritants, dermal sensitizers and other respiratory sensitizers are needed to further evaluate the overall sensitivity and selectivity of this novel protocol.
authors: Institute of Environmental Toxicology, Ibaraki, Japan. fukuyama@iet.or.jp
authors: Tomoki
authors: T
authors: Fukuyama
authors: Yukari
authors: Y
authors: Tajima
authors: Hideo
authors: H
authors: Ueda
authors: Koichi
authors: K
authors: Hayashi
authors: Yasufumi
authors: Y
authors: Shutoh
authors: Toru R
authors: TR
authors: Saito
authors: Takanori
authors: T
authors: Harada
authors: Tadashi
authors: T
authors: Kosaka
mesh_terms: D000818:Animals; D000943:Antigens, Differentiation / Q000276:immunology / Q000378:metabolism; D001402:B-Lymphocytes / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D000939:Epitopes; D005260:Female; D007115:Immunization Schedule; D007073:Immunoglobulin E / Q000097:blood; D016753:Interleukin-10 / Q000378:metabolism; D018793:Interleukin-13 / Q000378:metabolism; D018655:Lymphocyte Count; D051379:Mice; D008807:Mice, Inbred BALB C; D010796:Phthalic Anhydrides / Q000008:administration & dosage / Q000009:adverse effects; D012130:Respiratory Hypersensitivity / Q000097:blood / Q000139:chemically induced / Q000276:immunology* / Q000473:pathology; D018418:Th2 Cells / Q000276:immunology / Q000378:metabolism* / Q000473:pathology
chemical_list: D000943:Antigens, Differentiation; D000939:Epitopes; D018793:Interleukin-13; D010796:Phthalic Anhydrides; D016753:Interleukin-10; D007073:Immunoglobulin E; C015559:trimellitic anhydride