Abstract
Background: IL-11 is a pleiotropic cytokine produced by a variety of stromal cells. Targeted overexpression of this cytokine in mice results in a remodeling of the airways and the development of airway hyperresponsiveness and airway obstruction. Objectives: Because these alterations mimic important pathologic and physiologic changes in the airways of some asthmatic patients, we investigated the expression of IL-11 messenger RNA (mRNA) within the airways of patients with mild to severe asthma and nonasthmatic control subjects. Methods: Fiberoptic bronchoscopy to obtain bronchial biopsy specimens was performed on patients with mild (n = 13), moderate (n = 10), and severe (n = 9) asthma and on nonasthmatic control subjects (n = 9). Results: These patients differed in their extent of airway fibrosis with types I and III collagens being noted in greater quantities in the biopsy specimens from the severe and moderate asthmatics than in those from controls (P < .05). IL-11 mRNA expression was observed in the epithelial and subepithelial layers of asthmatic and nonasthmatic control subjects. The number of cells within the epithelium and subepithelium expressing IL-11 mRNA was greater in those with moderate and severe asthma compared with mild asthma and nonasthmatic subjects (P < .001). There were also greater numbers of IL-11 mRNA-positive cells within the subepithelium in severe compared with moderate asthma (P < .001). Immunostaining for IL-11 within the airway tissues confirmed translation of the mRNA into IL-11–immunoreactive protein in airway epithelial cells. Colocalization of IL-11 mRNA and immunoreactivity with resident inflammatory cells demonstrated that this cytokine was also expressed by major basic protein–positive eosinophils. Conclusion: These results suggest that IL-11 is involved in the chronic remodeling seen in asthmatic airways and is associated with increasing severity of the disease. (J Allergy Clin Immunol 2000;105:232-8.)
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