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Originally published online as doi:10.2353/ajpath.2009.080223 on April 23, 2009

Published online before print April 23, 2009
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(American Journal of Pathology. 2009;174:2225-2233.)
© 2009 American Society for Investigative Pathology
DOI: 10.2353/ajpath.2009.080223

Establishment of Experimental Eosinophilic Vasculitis by IgE-Mediated Cutaneous Reverse Passive Arthus Reaction

Takayuki Ishii*, Tomoyuki Fujita*, Takashi Matsushita*, Koichi Yanaba*, Minoru Hasegawa*, Hiroko Nakashima{dagger}, Fumihide Ogawa{ddagger}, Kazuhiro Shimizu{ddagger}, Kazuhiko Takehara*, Thomas F. Tedder§, Shinichi Sato{ddagger} and Manabu Fujimoto*

From the Department of Dermatology,* Kanazawa University Graduate School of Medical Science, Kanazawa, Japan; the Department of Dermatology,{dagger} Faculty of Medicine, University of Tokyo, Tokyo, Japan; the Department of Dermatology,{ddagger} Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan; and the Department of Immunology,§ Duke University Medical Center, Durham, North Carolina

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.






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