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

Korsgren, Magnus LU ; Kallstrom, L; Uller, Lena LU ; Bjerke, T; Sundler, Frank LU ; Persson, Carl LU and Korsgren, O (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)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Mediators of Inflammation
volume
9
issue
1
pages
15 - 23
publisher
Hindawi Publishing Corporation
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
2009-07-30 15:37:04
date last changed
2016-11-24 14:55:48
@misc{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    = {ARRAY(0xc69e508)},
  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},
  volume       = {9},
  year         = {2000},
}