title: Establishment of experimental eosinophilic vasculitis by IgE-mediated cutaneous reverse passive arthus reaction.
abstract: Prominent eosinophil infiltration is a characteristic of some forms of vasculitis, such as Churg-Strauss syndrome, also known as allergic granulomatous vasculitis. In the current study, we established a mouse model of cutaneous eosinophilic vasculitis by the cutaneous reverse passive Arthus reaction using IgE injection instead of IgG. Wild-type C57BL/6 mice were injected with IgE anti-trinitrophenyl antibodies, followed immediately by intravenous administration of trinitrophenyl bovine serum albumin. IgE-mediated immune complex challenge induced substantial hemorrhage with marked infiltration of eosinophils in which neutrophils, mast cells, and macrophages were also mixed. This finding contrasted remarkably with the neutrophil-dominant infiltration pattern in IgG-mediated immune complex challenge. In the lesion, the expression level of monocyte chemotactic protein-3 was increased, and anti-monocyte chemotactic protein-3 treatment resulted in a significant but incomplete blockade of eosinophil recruitment. Furthermore, mice lacking E-selectin, P-selectin, L-selectin, or intercellular adhesion molecule-1, as well as wild-type mice that received anti-vascular cell adhesion molecule-1-blocking antibodies were assessed for the IgE-mediated Arthus reaction. After 24 hours, the loss of P-selectin resulted in a significant reduction in eosinophil accumulation compared with both wild-type mice and other mouse mutants. Collectively, the Fc class of immunoglobulins, which forms these immune complexes, critically determines the disease manifestation of vasculitis. The IgE-mediated cutaneous reverse passive Arthus reaction may serve as an experimental model for cutaneous eosinophilic infiltration in vasculitis as well as in other diseases.
authors.affiliation: Department of Dermatology, Kanazawa University Graduate School of Medical Science, 13-1 Takaramachi, Kanazawa, Ishikawa 920-8641, Japan.
authors.forename: Takayuki
authors.initials: T
authors.lastname: Ishii
authors.forename: Tomoyuki
authors.initials: T
authors.lastname: Fujita
authors.forename: Takashi
authors.initials: T
authors.lastname: Matsushita
authors.forename: Koichi
authors.initials: K
authors.lastname: Yanaba
authors.forename: Minoru
authors.initials: M
authors.lastname: Hasegawa
authors.forename: Hiroko
authors.initials: H
authors.lastname: Nakashima
authors.forename: Fumihide
authors.initials: F
authors.lastname: Ogawa
authors.forename: Kazuhiro
authors.initials: K
authors.lastname: Shimizu
authors.forename: Kazuhiko
authors.initials: K
authors.lastname: Takehara
authors.forename: Thomas F
authors.initials: TF
authors.lastname: Tedder
authors.forename: Shinichi
authors.initials: S
authors.lastname: Sato
authors.forename: Manabu
authors.initials: M
authors.lastname: Fujimoto
mesh_terms: D000818:Animals; D000936:Antigen-Antibody Complex; D001183:Arthus Reaction / Q000276:immunology*; D004195:Disease Models, Animal; D019040:E-Selectin / Q000276:immunology; D004802:Eosinophilia / Q000276:immunology* / Q000473:pathology; D007073:Immunoglobulin E / Q000276:immunology*; D007074:Immunoglobulin G / Q000276:immunology; D007150:Immunohistochemistry; D018799:Intercellular Adhesion Molecule-1 / Q000276:immunology; D019041:L-Selectin / Q000276:immunology; D051379:Mice; D008810:Mice, Inbred C57BL; D019007:P-Selectin / Q000276:immunology; D020133:Reverse Transcriptase Polymerase Chain Reaction; D012871:Skin Diseases / Q000276:immunology* / Q000473:pathology; D018366:Vasculitis, Leukocytoclastic, Cutaneous / Q000276:immunology* / Q000473:pathology
chemical_list: D000936:Antigen-Antibody Complex; D019040:E-Selectin; D007074:Immunoglobulin G; D019007:P-Selectin; D018799:Intercellular Adhesion Molecule-1; D019041:L-Selectin; D007073:Immunoglobulin E