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© The Rockefeller University Press, 0022-1007/1997/8/601/ $5.00
The Journal of Experimental Medicine, Volume 186, Number 4, August 18, 1997 601-612

Article

Kinetics of Eotaxin Generation and Its Relationship to Eosinophil Accumulation in Allergic Airways Disease: Analysis in a Guinea Pig Model In Vivo

Alison A. Humbles*, Dolores M. Conroy*, Sylvie Marleau*, Sara M. Rankin*, Roger T. Palframan*, Amanda E.I. Proudfoot§, Timothy N.C. Wells§, Dechun Li{ddagger}, Peter K. Jeffery{ddagger}, David A. Griffiths-Johnson*, Timothy J. Williams*, and Peter J. Jose*

From the * Department of Applied Pharmacology and the {ddagger} Department of Lung Pathology, Imperial College School of Medicine at the National Heart and Lung Institute, London SW3 6LY, United Kingdom; and § Glaxo-Wellcome Molecular, Geneva, Switzerland

Challenge of the airways of sensitized guinea pigs with aerosolized ovalbumin resulted in an early phase of microvascular protein leakage and a delayed phase of eosinophil accumulation in the airway lumen, as measured using bronchoalveolar lavage (BAL). Immunoreactive eotaxin levels rose in airway tissue and BAL fluid to a peak at 6 h falling to low levels by 12 h. Eosinophil numbers in the tissue correlated with eotaxin levels until 6 h but eosinophils persisted until the last measurement time point at 24 h. In contrast, few eosinophils appeared in BAL over the first 12 h, major trafficking through the airway epithelium occurring at 12–24 h when eotaxin levels were low. Constitutive eotaxin was present in BAL fluid. Both constitutive and allergen-induced eosinophil chemoattractant activity in BAL fluid was neutralized by an antibody to eotaxin. Allergen-induced eotaxin appeared to be mainly in airway epithelium and macrophages, as detected by immunostaining. Allergen challenge of the lung resulted in a rapid release of bone marrow eosinophils into the blood. An antibody to IL-5 suppressed bone marrow eosinophil release and lung eosinophilia, without affecting lung eotaxin levels. Thus, IL-5 and eotaxin appear to cooperate in mediating a rapid transfer of eosinophils from the bone marrow to the lung in response to allergen challenge.

Address correspondence to Professor T.J. Williams, Applied Pharmacology, Imperial College School of Medicine at the National Heart and Lung Institute, Dovehouse Street, London SW3 6LY, United Kingdom. Phone: 171-351-8170; FAX: 171-351-8270; E-mail: tim.williams{at}ic.ac.uk. Alison Humbles's present address is Ina Sue Perlmutter Laboratory, Pulmonary Department, Children's Hospital, Harvard Medical School, Boston, MA 02115.

1 Abbreviations used in this paper: BAL, bronchoalveolar lavage; EPO, eosinophil peroxidase; i.d., intradermally.


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