Remodeling of extra-bronchial lung vasculature following allergic airway inflammation.
Rydell-Törmänen, Kristina LU
; Uller, Lena
LU
and Erjefält, Jonas
LU
(2008)
In Respiratory Research
9(18, FEb 8).
- 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... (More)
- 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. CONCLUSION: 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. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/1042119
- author
- Rydell-Törmänen, Kristina
LU
; Uller, Lena
LU
and Erjefält, Jonas
LU
- organization
- publishing date
- 2008
- type
- Contribution to journal
- publication status
- published
- subject
- in
- Respiratory Research
- volume
- 9
- issue
- 18, FEb 8
- article number
- 18
- publisher
- BioMed Central (BMC)
- external identifiers
-
- pmid:18261211
- wos:000253797000001
- scopus:41149092973
- ISSN
- 1465-9921
- DOI
- 10.1186/1465-9921-9-18
- language
- English
- LU publication?
- yes
- id
- e85b2b3d-d52c-4ae7-b3c3-e1c8ca8d2e91 (old id 1042119)
- alternative location
- http://www.ncbi.nlm.nih.gov/pubmed/18261211?dopt=Abstract
- date added to LUP
- 2016-04-04 08:52:43
- date last changed
- 2022-01-29 07:22:31
@article{e85b2b3d-d52c-4ae7-b3c3-e1c8ca8d2e91,
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. CONCLUSION: 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.}},
author = {{Rydell-Törmänen, Kristina and Uller, Lena and Erjefält, Jonas}},
issn = {{1465-9921}},
language = {{eng}},
number = {{18, FEb 8}},
publisher = {{BioMed Central (BMC)}},
series = {{Respiratory Research}},
title = {{Remodeling of extra-bronchial lung vasculature following allergic airway inflammation.}},
url = {{https://lup.lub.lu.se/search/files/5200570/1055614.pdf}},
doi = {{10.1186/1465-9921-9-18}},
volume = {{9}},
year = {{2008}},
}