Role for macrophage migration inhibitory factor in asthma
Author(s) -
Yuka Mizue,
Samina Ghani,
Lin Leng,
Courtney McDonald,
Philip Kong,
John A. Baugh,
Stephen J. Lane,
Joseph Craft,
Jun Nishihira,
Seamas C. Donnelly,
Zhou Zhu,
Richard Bucala
Publication year - 2005
Publication title -
proceedings of the national academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.011
H-Index - 771
eISSN - 1091-6490
pISSN - 0027-8424
DOI - 10.1073/pnas.0507189102
Subject(s) - macrophage migration inhibitory factor , immunology , asthma , ovalbumin , bronchoalveolar lavage , medicine , eosinophil , immunoglobulin e , cytokine , inflammation , eosinophilia , antigen , lung , antibody
Macrophage migration inhibitory factor (MIF) is an immunologic regulator that is expressed in inflammatory and autoimmune disorders. We investigated MIF's role in asthma using genetic approaches in a mouse model and in a cohort of asthma patients. Mice genetically deficient in MIF that were primed and aerosol-challenged with ovalbumin showed less pulmonary inflammation and lower airway hyperresponsiveness than genetically matched, wild-type controls. MIF deficiency also resulted in lower titers of specific IgE, IgG(1), and IgG(2a), and decreased pulmonary, T(H)2 cytokine levels. IL-5 concentrations were lower and corresponded to decreased eosinophil numbers in bronchoalveolar lavage fluid. T cell studies also showed a lower level of antigen-specific responses in MIF-KO versus wild-type mice. In an analysis of 151 white patients with mild, moderate, or severe asthma (Global Initiative for Asthma criteria), a significant association was found between mild asthma and the low-expression, 5-CATT MIF allele. Pharmacologic inhibition of MIF may be beneficial and could be guided by the MIF genotype of affected individuals.
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