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Blood, 15 November 2000, Vol. 96, No. 10, pp. 3601-3609
PHAGOCYTES
VCAM-1 has a tissue-specific role in mediating
interleukin-4-induced eosinophil accumulation in rat models: evidence
for a dissociation between endothelial-cell VCAM-1
expression and a functional role in eosinophil migration
Karen Y. Larbi,
Andrew R. Allen,
Frederick W. K. Tam,
Dorian O. Haskard,
Roy R. Lobb,
Patricia M. R. Silva, and
Sussan Nourshargh
From the BHF Cardiovascular Medicine Unit, Imperial
College School of Medicine at the National Heart and Lung Institute,
London, United Kingdom; the Renal Section, Division of Medicine,
Imperial College School of Medicine, London, United Kingdom; Biogen
Inc, Cambridge, MA; and Fiocruz, Rio de Janeiro, Brazil.
Eosinophil accumulation has been associated with the pathogenesis
of numerous allergic inflammatory disorders. Despite the great interest
in this response, many aspects of eosinophil accumulation remain
unknown. This is particularly true with respect to tissue-specific mechanisms that may regulate the accumulation of eosinophils in different organs. This study addressed this issue by investigating and
comparing the roles of  4-integrins and vascular cell
adhesion molecule 1 (VCAM-1) adhesion pathways in interleukin 4 (IL-4)-induced eosinophil accumulation in 2 different rat models of
inflammation, namely pleural and cutaneous inflammation. Similar to our
previous findings in studies in rat skin, locally administered IL-4
induced a time- and dose-dependent accumulation of eosinophils in rat pleural cavities, a response that was associated with generation of the
chemokine eotaxin. The IL-4-induced eosinophil accumulation in skin
and pleural cavities was totally inhibited by an antirat 4-integrins monoclonal antibody (mAb) (TA-2). In
contrast, whereas an antirat VCAM-1 mAb (5F10) totally blocked the
response in skin, IL-4-induced eosinophil accumulation in rat pleural
cavities was not affected by VCAM-1 blockade. A radiolabeled mAb
technique demonstrated that endothelial-cell VCAM-1 expression was
induced in response to IL-4 in both skin and pleural membrane. The
results indicate that although endothelial-cell VCAM-1 is present in
skin and pleura, a functional role for it in IL-4-induced eosinophil accumulation was evident only in skin. These findings suggest the
existence of tissue-specific adhesive mechanisms in regulating leukocyte migration in vivo and demonstrate a dissociation between VCAM-1 expression and eosinophil accumulation.
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