Mediators of Inflammation

Mediators of Inflammation / 2000 / Article

Open Access

Volume 9 |Article ID 298708 | https://doi.org/10.1080/09629350050024339

M. Korsgren, L. Källström, L. Uller, T. Bjerke, F. Sundler, C. G. A. Persson, O. Korsgren, "Role of macrophage migration inhibitory factor (MIF) in allergic and endotoxin-induced airway inflammation in mice", Mediators of Inflammation, vol. 9, Article ID 298708, 9 pages, 2000. https://doi.org/10.1080/09629350050024339

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

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.

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.


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