Allergic airway inflammation initiates long-term vascular remodeling of the pulmonary circulation.
BACKGROUND
Asthma and allergic airway inflammation are associated with persistent structural alterations in the bronchi, i.e. airway remodeling. Previous studies have shown that during allergic airway inflammation, similar structural alterations may also be evoked in the pulmonary circulation. However, it remained unknown whether remodeling of the pulmonary circulation is as persistent as airway remodeling. The aim of this study is to investigate the reversibility and resolution of vascular remodeling, induced by allergic airway inflammation.


METHODS
A validated mouse model of allergic airway inflammation, utilizing ovalbumin as allergen, was employed. Animals were sacrificed 1 day, 1 week or 1 month after the last allergen exposure, and different parameters of remodeling (smooth muscle mass, proliferation of smooth muscle cells and endothelial cells as well as number of myofibroblasts and procollagen-I-producing cells) were investigated and quantified histologically.


RESULTS
Allergen exposure resulted in allergic airway inflammation characterized by a transient leukocyte infiltration and in structural alterations in both airway and vascular compartments. The increase in vascular smooth muscle mass and endothelial proliferation persisted at 1 month after the last allergen exposure. The other parameters and cellular inflammatory response returned to baseline within 1 month after the last allergen challenge.


CONCLUSIONS
Based on the findings in this study, we conclude that acute allergic airway inflammation, although being initiated from the airways, is able to evoke similar long-term structural alterations in pulmonary vessels as described for bronchi.
Rydell-Törmänen
Kristina
K
Division of Vascular and Airway Research, Department of Experimental Medical Science, Lund University, Lund, Sweden. Kristina.Rydell-Tormanen@med.lu.se
Uller
Lena
L
Erjefält
Jonas S
JS
D000485:Allergens / Q000276:immunology; D000818:Animals; D001249:Asthma / Q000276:immunology / Q000378:metabolism / Q000473:pathology*; D049109:Cell Proliferation; D004730:Endothelium, Vascular / Q000276:immunology / Q000473:pathology*; D004802:Eosinophilia / Q000276:immunology / Q000473:pathology; D005260:Female; D008168:Lung / Q000098:blood supply* / Q000276:immunology / Q000473:pathology*; D051379:Mice; D008807:Mice, Inbred BALB C; D032389:Myocytes, Smooth Muscle / Q000276:immunology; D010047:Ovalbumin / Q000276:immunology; D011014:Pneumonia / Q000276:immunology / Q000473:pathology*; D011347:Procollagen / Q000096:biosynthesis / Q000276:immunology; D011652:Pulmonary Circulation / Q000276:immunology*
D000485:Allergens; D011347:Procollagen; D010047:Ovalbumin