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Published ahead of print on September 24, 2004, doi:10.1164/rccm.200406-698OC
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American Journal of Respiratory and Critical Care Medicine Vol 171. pp. 19-25, (2005)
© 2005 American Thoracic Society
doi: 10.1164/rccm.200406-698OC

Original Article

Allergen Exposure of Mouse Airways Evokes Remodeling of both Bronchi and Large Pulmonary Vessels

Kristina Rydell Törmänen, Lena Uller, Carl G. A. Persson and Jonas S. Erjefält

Department of Physiological Sciences and Department of Clinical Pharmacology, Lund University Hospital, Lund, Sweden

Correspondence and requests for reprints should be addressed to Kristina Rydell Törmänen, M.Sc., Department of Physiological Sciences, BMC F10, Lund University, 221 84 Lund, Sweden. E-mail: kristina.rydell{at}mphy.lu.se

Remodeling of airway structures is a well-documented feature of allergic airway inflammation. To investigate whether bronchial remodeling is associated with remodeling of adjacent pulmonary vessels, sensitized mice were subjected to repeated ovalbumin inhalations, and bronchi and pulmonary vessels were subjected to histologic analysis. Allergen challenges induced peribronchial as well as perivascular eosinophilia. Remodeling of systemic airway microcirculation, as studied in tracheal whole-mount preparations, revealed an allergen-induced increase in both the diameter and length of the airway microvessels. Immunostaining for {alpha}-smooth muscle actin disclosed an increase in smooth muscle mass in both bronchi and large pulmonary vessels. Both bronchi and pulmonary vessels also displayed increased expression of procollagen I and procollagen III. Staining for proliferating cell nuclear antigen revealed increased proliferation of bronchial epithelial and smooth muscle cells as well as pulmonary vascular endothelial and smooth muscle cells. We conclude that central features of remodeling that take place in allergen-exposed airways are present also in the pulmonary vessels. The significance of this finding with respect to occurrence in disease, pathophysiologic importance, and involved mechanisms warrants further investigation.

Key Words: animal model • asthma • eosinophils • vascular remodeling




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