Role of macrophage migration inhibitory factor (MIF) in allergic and endotoxin-induced airway inflammation in mice
(2000) In Mediators of Inflammation 9(1). p.15-23- 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 lipopolysaccharide (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... (More)
- 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 lipopolysaccharide (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-alpha (TNF-alpha) and macrophage inflammatory protein-1alpha (MIP-1alpha). 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. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/1296769
- author
- Korsgren, Magnus LU ; Kallstrom, L ; Uller, Lena LU ; Bjerke, T ; Sundler, Frank LU ; Persson, Carl LU and Korsgren, O
- organization
- publishing date
- 2000
- type
- Contribution to journal
- publication status
- published
- subject
- in
- Mediators of Inflammation
- volume
- 9
- issue
- 1
- pages
- 15 - 23
- publisher
- Hindawi Limited
- external identifiers
-
- scopus:0034043154
- ISSN
- 0962-9351
- DOI
- 10.1080/09629350050024339
- language
- English
- LU publication?
- yes
- id
- ef93b8fb-a007-4a37-ade8-e8f1ef3b72e9 (old id 1296769)
- date added to LUP
- 2016-04-04 10:20:28
- date last changed
- 2022-01-29 20:09:54
@article{ef93b8fb-a007-4a37-ade8-e8f1ef3b72e9, 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 lipopolysaccharide (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-alpha (TNF-alpha) and macrophage inflammatory protein-1alpha (MIP-1alpha). 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.}}, author = {{Korsgren, Magnus and Kallstrom, L and Uller, Lena and Bjerke, T and Sundler, Frank and Persson, Carl and Korsgren, O}}, issn = {{0962-9351}}, language = {{eng}}, number = {{1}}, pages = {{15--23}}, publisher = {{Hindawi Limited}}, series = {{Mediators of Inflammation}}, title = {{Role of macrophage migration inhibitory factor (MIF) in allergic and endotoxin-induced airway inflammation in mice}}, url = {{http://dx.doi.org/10.1080/09629350050024339}}, doi = {{10.1080/09629350050024339}}, volume = {{9}}, year = {{2000}}, }