Asthma is a clinical syndrome of airway inflammation, excessive response,
and airflow obstruction to the lungs. Patients with asthma produce migration
inhibitory factor (MIF), a gene product that regulates immunity, in their serum
and in the fluid that lines their lungs.
“Asthma patients who have high production variants of the macrophage
migration inhibitory factor gene (MIF) are more likely to have severe disease,” Bucala
said.
The study by Bucala and his colleagues in Dublin, Ireland, included experiments
in mice that are resistant to developing asthma because they lack the gene,
and an examination of a human population in Dublin chosen for their similar
ethnic and geographic identity.
When challenged with a trigger for their asthma attack, the genetically deficient
mice had less pulmonary inflammation and lower airway hyper-responsiveness
than genetically matched, wild-type control mice. Similarly, in an analysis
of 151 Caucasian patients with mild, moderate and severe asthma, there was
a significant association between mild asthma and the low expression of MIF.
“These results support an important role for MIF in the pathogenesis
of human asthma,” Bucala said. “A drug treatment to lower MIF
in patients may be beneficial and could be guided by the MIF genotype of
affected
individuals.”
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