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

M. Korsgren ； L. Kallstrom ； L. Uller ； T. Bjerke ； F. Sundler ； C. G. A. Persson ； O. Korsgren

《Mediators of Inflammation》 2000卷 (2000/12) Pp. 15-23

https://doi.org/10.1080/09629350050024339

摘要

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 se rum 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 mode l 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 r educe BALF levels of tumor necros is facto r- a (TNF- α) and macrophage inflammatory protein -1α(MIP-1α). 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.

關鍵字

Macrophage migration inhibitory factor (MIF) ； Allergen-induced eosinophilia ； LPS-induced neutrophilia ； Mouse models of inflammatory lung diseases