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 Dis. (COPD). Hence, we examined effects of MIF immunoneutralization on the Devt. 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-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.
CITATION STYLE
Korsgren, M., Källström, L., Uller, L., Bjerke, T., Sundler, F., Persson, C. G. A., & Korsgren, O. (2000). Role of macrophage migration inhibitory factor (MIF) in allergic and endotoxin-induced airway inflammation in mice. Mediators of Inflammation, 9(1), 15–23. https://doi.org/10.1080/09629350050024339
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