title: Remodeling of extra-bronchial lung vasculature following allergic airway inflammation.
abstract: BACKGROUND
  We previously observed that allergen-exposed mice exhibit remodeling of large bronchial-associated blood vessels. The aim of the study was to examine whether vascular remodeling occurs also in vessels where a spill-over effect of bronchial remodeling molecules is less likely.
  
  
  METHODS
  We used an established mouse model of allergic airway inflammation, where an allergic airway inflammation is triggered by inhalations of OVA. Remodeling of bronchial un-associated vessels was determined histologically by staining for alpha-smooth muscle actin, procollagen I, Ki67 and von Willebrand-factor. Myofibroblasts were defined as and visualized by double staining for alpha-smooth muscle actin and procollagen I. For quantification the blood vessels were divided, based on length of basement membrane, into groups; small (</=250 mum) and mid-sized (250-500 mum).
  
  
  RESULTS
  We discovered marked remodeling in solitary small and mid-sized blood vessels. Smooth muscle mass increased significantly as did the number of proliferating smooth muscle and endothelial cells. The changes were similar to those previously seen in large bronchial-associated vessels. Additionally, normally poorly muscularized blood vessels changed phenotype to a more muscularized type and the number of myofibroblasts around the small and mid-sized vessels increased following allergen challenge.
  
  
  CONCLUSIONS
  We demonstrate that allergic airway inflammation in mice is accompanied by remodeling of small and mid-sized pulmonary blood vessels some distance away (at least 150 mum) from the allergen-exposed bronchi. The present findings suggest the possibility that allergic airway inflammation may cause such vascular remodeling as previously associated with lung inflammatory conditions involving a risk for development of pulmonary hypertension.
authors.affiliation: Div, Vascular and Airway Research, Dept, Experimental Medical Science, Lund University, Lund, Sweden. Kristina.Rydell-Tormanen@med.lu.se
authors.forename: Kristina
authors.initials: K
authors.lastname: Rydell-Törmänen
authors.forename: Lena
authors.initials: L
authors.lastname: Uller
authors.forename: Jonas S
authors.initials: JS
authors.lastname: Erjefält
mesh_terms: D000485:Allergens; D000818:Animals; D001980:Bronchi / Q000098:blood supply / Q000503:physiopathology*; D001985:Bronchial Provocation Tests; D002199:Capillary Permeability; D004195:Disease Models, Animal; D004802:Eosinophilia / Q000503:physiopathology*; D005260:Female; D051379:Mice; D008807:Mice, Inbred BALB C; D008833:Microcirculation / Q000276:immunology / Q000502:physiology; D009131:Muscle, Smooth, Vascular / Q000503:physiopathology*; D010047:Ovalbumin; D011652:Pulmonary Circulation / Q000502:physiology; D011897:Random Allocation; D012016:Reference Values; D012038:Regeneration / Q000502:physiology; D012130:Respiratory Hypersensitivity / Q000139:chemically induced / Q000503:physiopathology*; D020545:Respiratory Mucosa / Q000473:pathology / Q000503:physiopathology; D012680:Sensitivity and Specificity
chemical_list: D000485:Allergens; D010047:Ovalbumin