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and 4 Integrin/VCAM-1 Adhesion Pathways1
*
Imperial College School of Medicine at the National Heart and Lung Institute, London, United Kingdom;
Biogen, Cambridge, MA 02142; and
Kennedy Institute of Rheumatology, London, United Kingdom
IL-4 has been implicated in the pathogenesis of a number of
allergic inflammatory disease states where the accumulation of
eosinophils is a prominant feature. The aim of the present study was to
use an isotopic in vivo model to investigate the ability of recombinant
rat IL-4 in inducing eosinophil accumulation in rat skin.
111In-eosinophil accumulation in response to
intradermally injected IL-4 was measured during 0 to 4 h, 24 to
28 h, and 48 to 52 h. Accumulation was detected during the
first two periods, but not at the later time point. The accumulation
during 24 to 28 h, which was dose dependent, was investigated in
detail. Administration i.v. of an anti-rat VCAM-1 mAb, but not an
anti-rat ICAM-1 mAb, inhibited the accumulation of
111In-eosinophils induced by IL-4 (maximum inhibition,
80%). Further, when the 111In-eosinophils were pretreated
in vitro with an anti-ß2 integrin mAb, an
anti-
4 integrin mAb, or a combination of both mAbs,
before their injection into recipient rats, the IL-4-induced cell
accumulation was inhibited by 63, 60, and 74%, respectively. Finally,
coadministration of IL-4 with the soluble TNF receptor (p55)-IgG fusion
protein significantly reduced the 111In-eosinophil
accumulation induced by the cytokine, and TNF- was detected in
IL-4-injected skin sites by both immunostaining and bioassay. Our
results demonstrate that IL-4 is a potent inducer of eosinophil
accumulation in vivo, the response being dependent on the endogenous
generation of TNF-, ß2 integrins, and 4
integrin/VCAM-1 interactions.
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