MONDAY, Feb. 23 (HealthDay News) -- The antifibrotic peptide hormone relaxin reverses lung fibrosis and airway hyperresponsiveness in a mouse model of asthma, according to the results of a study published online Feb. 12 in Endocrinology.
Simon G. Royce, from the Royal Children's Hospital in Melbourne, Victoria, Australia, and colleagues examined relaxin expression and the effect of relaxin treatment in a mouse model of allergic airways disease. Mice deficient in relaxin undergo airway remodeling, they note, and exaggerated airway remodeling in models of allergic airways disease.
The investigators found that the mice had significantly lower relaxin expression in lung tissue than normal mice. Systemic relaxin treatment reversed subepithelial collagen deposition, epithelial thickening and airway hyperresponsiveness, they note. Relaxin had no significant effect on airway inflammation or the number of goblet cells. Levels of matrix metalloproteinase-2, which degrades collagen and had been previously shown to play a role in asthma, were also higher after relaxin treatment, the researchers report.
"Endogenous relaxin expression is decreased in murine allergic airways disease, while exogenous relaxin represents a novel treatment capable of reversing established airway remodeling and airway hyperresponsiveness," Royce and colleagues conclude.
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