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Allergen challenge-induced extravasation of plasma in mouse airways

Erjefält, Jonas LU ; Andersson, P; Gustafsson, B; Korsgren, M; Sonmark, B and Persson, C G (1998) In Clinical and Experimental Allergy 28(8). p.1013-1020
Abstract
BACKGROUND: Mouse models are extensively used to study genetic and immunological mechanisms of potential importance to inflammatory airway diseases, e.g. asthma. However, the airway pathophysiology in allergic mice has received less attention. For example, plasma extravasation and the ensuing tissue-deposition of plasma proteins, which is a hallmark of inflammation, has not been examined in allergic mice. OBJECTIVE: This study aims to examine the vascular permeability and the distribution of plasma proteins in mouse airways following exposure to allergen and serotonin. METHODS: Extravasated plasma was quantified by a dual isotop technique using intravascular (131I-albumin) and extrasvascular (125I-albumin) plasma tracers. Histological... (More)
BACKGROUND: Mouse models are extensively used to study genetic and immunological mechanisms of potential importance to inflammatory airway diseases, e.g. asthma. However, the airway pathophysiology in allergic mice has received less attention. For example, plasma extravasation and the ensuing tissue-deposition of plasma proteins, which is a hallmark of inflammation, has not been examined in allergic mice. OBJECTIVE: This study aims to examine the vascular permeability and the distribution of plasma proteins in mouse airways following exposure to allergen and serotonin. METHODS: Extravasated plasma was quantified by a dual isotop technique using intravascular (131I-albumin) and extrasvascular (125I-albumin) plasma tracers. Histological visualization of fibrinogen and colloidal gold revealed the tissue distribution of extravasated plasma. RESULTS: Allergen aerosol exposure (3% OVA, 15min) of sensitized animals resulted in a marked plasma extravasation response in the trachea (P < 0.01) and the bronchi but not in the lung parenchyma. A similar extravasation response was induced by serotonin (P<0.001). Extravasating vessels (assessed by Monastral blue dye) were identified as intercartilaginous venules. Extravasated plasma abounded in the subepithelial tissue but was absent in the epithelium and airway lumen. The allergen-induced response was dose-dependently inhibited by iv administration of formoterol (P < 0.001), a vascular antipermeability agent. CONCLUSION: The present study demonstrates that serotonin and allergen challenge of sensitized mice increase airway venular permeability to cause transient extravasation and lamina propria distribution of plasma in the large airways. We suggest that the extravasation response is a useful measure of the intensity and the distribution of active inflammation (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
extravasation, plasma, mice, ovalbumin, serotonin, formoterol
in
Clinical and Experimental Allergy
volume
28
issue
8
pages
1013 - 1020
publisher
Wiley-Blackwell
external identifiers
  • pmid:9756207
  • scopus:0031662294
ISSN
1365-2222
DOI
10.1046/j.1365-2222.1998.00372.x
language
English
LU publication?
yes
id
8ffc3ef7-2f97-402c-ab55-830a08e88cee (old id 1113946)
date added to LUP
2008-07-16 14:12:44
date last changed
2017-01-01 04:39:50
@article{8ffc3ef7-2f97-402c-ab55-830a08e88cee,
  abstract     = {BACKGROUND: Mouse models are extensively used to study genetic and immunological mechanisms of potential importance to inflammatory airway diseases, e.g. asthma. However, the airway pathophysiology in allergic mice has received less attention. For example, plasma extravasation and the ensuing tissue-deposition of plasma proteins, which is a hallmark of inflammation, has not been examined in allergic mice. OBJECTIVE: This study aims to examine the vascular permeability and the distribution of plasma proteins in mouse airways following exposure to allergen and serotonin. METHODS: Extravasated plasma was quantified by a dual isotop technique using intravascular (131I-albumin) and extrasvascular (125I-albumin) plasma tracers. Histological visualization of fibrinogen and colloidal gold revealed the tissue distribution of extravasated plasma. RESULTS: Allergen aerosol exposure (3% OVA, 15min) of sensitized animals resulted in a marked plasma extravasation response in the trachea (P &lt; 0.01) and the bronchi but not in the lung parenchyma. A similar extravasation response was induced by serotonin (P&lt;0.001). Extravasating vessels (assessed by Monastral blue dye) were identified as intercartilaginous venules. Extravasated plasma abounded in the subepithelial tissue but was absent in the epithelium and airway lumen. The allergen-induced response was dose-dependently inhibited by iv administration of formoterol (P &lt; 0.001), a vascular antipermeability agent. CONCLUSION: The present study demonstrates that serotonin and allergen challenge of sensitized mice increase airway venular permeability to cause transient extravasation and lamina propria distribution of plasma in the large airways. We suggest that the extravasation response is a useful measure of the intensity and the distribution of active inflammation},
  author       = {Erjefält, Jonas and Andersson, P and Gustafsson, B and Korsgren, M and Sonmark, B and Persson, C G},
  issn         = {1365-2222},
  keyword      = {extravasation,plasma,mice,ovalbumin,serotonin,formoterol},
  language     = {eng},
  number       = {8},
  pages        = {1013--1020},
  publisher    = {Wiley-Blackwell},
  series       = {Clinical and Experimental Allergy},
  title        = {Allergen challenge-induced extravasation of plasma in mouse airways},
  url          = {http://dx.doi.org/10.1046/j.1365-2222.1998.00372.x},
  volume       = {28},
  year         = {1998},
}