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The Journal of Immunology, 1998, 160: 3569-3576.
Copyright © 1998 by The American Association of Immunologists

Human Eotaxin Induces {alpha}4 and ß2 Integrin-Dependent Eosinophil Accumulation in Rat Skin In Vivo: Delayed Generation of Eotaxin in Response to IL-41

Maria-Jesus Sanz2,*, Paul D. Ponath{dagger}, Charles R. Mackay{dagger}, Walter Newman{dagger}, Masayuki Miyasaka{ddagger}, Tayuka Tamatani{ddagger}, Brian F. Flanagan§, Roy R. Lobb, Timothy J. Williams*, Sussan Nourshargh* and Peter J. Jose3,*

* Leukocyte Biology Centre, Biomedical Sciences Division, Imperial College School of Medicine, London, United Kingdom; {dagger} Leukosite Inc., Cambridge, MA 02142; {ddagger} Department of Immunology, Tokyo Metropolitan Institute of Medical Science, Tokyo, Japan; § Department of Immunology, University of Liverpool, Liverpool, United Kingdom; and Biogen Inc., Cambridge, MA 02142

The CC chemokine eotaxin, originally purified from bronchoalveolar lavage fluid of sensitized guinea pigs following allergen challenge, is a potent eosinophil-selective chemoattractant. In the present study, we have used 111In-eosinophils and human eotaxin to characterize the profile of chemokine-induced eosinophil accumulation in vivo in rat skin. Intradermally injected eotaxin caused a dose-dependent accumulation of 111In-eosinophils. Time course studies indicated that the response was rapid, since all the accumulation occurred within the first 1 to 2 h of eotaxin injection. The i.v. administration of anti-intercellular adhesion molecule-1, anti-vascular cell adhesion molecule-1, or anti-{alpha}4 integrin mAbs significantly inhibited the eosinophil accumulation induced by 100 pmol of human eotaxin by 73, 43, and 67%, respectively. Further, when 111In-eosinophils were pretreated in vitro with anti-{alpha}4 integrin or anti-ß2 integrin mAbs, or with a combination of both mAbs, eotaxin-induced responses in vivo were reduced by 52, 49, and 68%, respectively. Eosinophil accumulation induced by intradermal IL-4, but not that induced by TNF-{alpha} or leukotriene B4, appeared to be mediated in part by endogenously generated eotaxin. Anti-eotaxin Abs significantly inhibited (54%) the later phases (24–28 h) but not the early phase (0–4 h) of the response to IL-4. This was consistent with eotaxin mRNA expression peaking at 18 h after IL-4 injection. Our findings show that human eotaxin is a potent inducer of eosinophil accumulation in vivo, this response being dependent on {alpha}4 integrin/vascular cell adhesion molecule-1 and ß2 integrin/intercellular adhesion molecule-1 adhesion pathways. Further, the eosinophil accumulation in response to IL-4 is partly mediated by endogenously generated eotaxin.




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