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* Department of Allergy and Clinical Immunology, Faculty of Medicine, Imperial College, National Heart and Lung Institute, London, United Kingdom; and
Department of Pharmacology, School of Pharmacy, Faculty of Medicine, Hebrew University of Jerusalem-Hadassah Medical School, Jerusalem, Israel
Several in vitro studies suggest that eosinophils may play a role
in fibrosis, remodeling, and repair processes associated with
IgE-mediated hypersensitivity. However, the relationship in vivo,
between allergen-induced tissue eosinophilia and markers of repair has
yet to be established in human atopic subjects. Using the
allergen-induced cutaneous late-phase reaction as a model of allergic
inflammation, we have tested the hypothesis that eosinophil-derived
TGF-
1 and IL-13 are temporarily associated with myofibroblast
formation and deposition of tenascin and procollagen I. Biopsies were
taken from atopic volunteers at 1, 3, 6, 24, 48, and 72 h after
intradermal allergen challenge and were examined by
immunohistochemistry. Following the peak of the late-phase reaction (6
h) there were persisting TGF-1+ eosinophils, 
-smooth
muscle actin+ myofibroblasts, tenascin immunoreactivity,
and procollagen-I+ cells 24–48 h postchallenge. Direct
evidence of generation of repair markers was obtained by coculture of
eosinophils and fibroblasts. This resulted in -smooth muscle actin
immunoreactivity that was inhibitable by neutralizing Abs to TGF- as
well as production of tenascin transcripts and protein product.
TGF-1 and IL-13 also induced tenascin expression. We conclude that
TGF-1 and IL-13, provided partially by eosinophils, contribute to
repair and remodeling events in allergic inflammation in human atopic
skin.
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