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Mediators of Inflammation
Volume 9, Issue 1, Pages 15-23
http://dx.doi.org/10.1080/09629350050024339

Role of macrophage migration inhibitory factor (MIF) in allergic and endotoxin-induced airway inflammation in mice

1Department of Physiological Sciences, Lund University Hospital, Lund 221 85, Sweden
2Clinical Pharmacology, Lund University Hospital, Lund 221 85, Sweden
3Department of Inflammation Pharmacology, AstraZeneca R&D Lund, Lund 221 87, Sweden
4Department of Clinical Immunology and Transfusion Medicine, Uppsala University Hospital, Uppsala 751 85, Sweden

Copyright © 2000 Hindawi Publishing Corporation. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Macrophage migration inhibitory factor (MIF) has recently been forwarded as a critical regulator of inflammatory conditions, and it has been hypothesized that MIF may have a role in the pathogenesis of asthma and chronic obstructive pulmonary disease (COPD). Hence, we examined effects of MIF immunoneutralization on the development of allergen-induced eosinophilic inflammation as well as on lipopolysaccaride (LPS)-induced neutrophilic inflammation in lungs of mice. Anti-MIF serum validated with respect to MIF neutralizing capacity or normal rabbit serum (NRS) was administered i.p. repeatedly during allergen aerosol exposure of ovalbumin (OVA)-immunized mice in an established model of allergic asthma, or once before instillation of a minimal dose of LPS into the airways of mice, a tentative model of COPD. Anti-MIF treatment did not affect the induced lung tissue eosinophilia or the cellular composition of bronchoalveolar lavage fluid (BALF) in the asthma model. Likewise, anti-MIF treatment did not affect the LPS-induced neutrophilia in lung tissue, BALF, or blood, nor did it reduce BALF levels of tumor necrosis factor-α (TNF-α) and macrophage inflammatory protein–1 α (MIP–1 α). The present data suggest that MIF is not critically important for allergen-induced eosinophilic, and LPS-induced neutrophilic responses in lungs of mice. These findings do not support a role of MIF inhibition in the treatment of inflammatory respiratory diseases.