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.