PMID- 18314535
OWN - NLM
STAT- MEDLINE
DCOM- 20080801
LR  - 20220410
IS  - 1535-4989 (Electronic)
IS  - 1044-1549 (Linking)
VI  - 39
IP  - 1
DP  - 2008 Jul
TI  - Induction of vascular remodeling in the lung by chronic house dust mite exposure.
PG  - 61-7
LID - 10.1165/rcmb.2007-0441OC [doi]
AB  - Structural changes to the lung are associated with chronic asthma. In addition to 
      alterations to the airway wall, asthma is associated with vascular modifications, 
      although this aspect of remodeling is poorly understood. We sought to evaluate 
      the character and kinetics of vascular remodeling in response to chronic 
      aeroallergen exposure. Because many ovalbumin-driven models used to investigate 
      allergic airway disease do so in the absence of persistent airway inflammation, 
      we used a protocol of chronic respiratory exposure to house dust mite extract 
      (HDME), which has been shown to induce persistent airway inflammation consistent 
      with that seen in humans with asthma. Mice were exposed to HDME intranasally for 
      7 or 20 consecutive weeks, and resolution of the inflammatory and remodeling 
      response to allergen was investigated 4 weeks after the end of a 7-week exposure 
      protocol. Measures of vascular remodeling, including total collagen deposition, 
      procollagen I production, endothelial and smooth muscle cell proliferation, 
      smooth muscle area, and presence of myofibroblasts, were investigated 
      histologically in lung vessels of different sizes and locations. We observed an 
      increase in total collagen content, which did not resolve upon cessation of 
      allergen exposure. Other parameters were significantly increased after 7 and/or 
      20 weeks of allergen exposure but returned to baseline after allergen withdrawal. 
      We conclude that respiratory HDME exposure induces airway remodeling and 
      pulmonary vascular remodeling, and, in accordance with airway remodeling, some 
      components of these structural changes may be irreversible.
FAU - Rydell-Tormanen, Kristina
AU  - Rydell-Tormanen K
AD  - Department of Experimental Medical Science, Division of Vascular and Airway 
      Research, BMC D12, S-22184 Lund, Sweden. Kristina.Rydell-Tormanen@med.lu.se
FAU - Johnson, Jill R
AU  - Johnson JR
FAU - Fattouh, Ramzi
AU  - Fattouh R
FAU - Jordana, Manel
AU  - Jordana M
FAU - Erjefalt, Jonas S
AU  - Erjefalt JS
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20080228
PL  - United States
TA  - Am J Respir Cell Mol Biol
JT  - American journal of respiratory cell and molecular biology
JID - 8917225
SB  - IM
MH  - Animals
MH  - Asthma/etiology
MH  - Bronchial Hyperreactivity/*etiology/parasitology/pathology
MH  - Bronchoalveolar Lavage
MH  - Cell Division
MH  - Female
MH  - Humans
MH  - Immunohistochemistry
MH  - Inflammation/*etiology/parasitology/pathology
MH  - Mice
MH  - Muscle, Smooth/pathology/physiopathology
MH  - Pulmonary Circulation/*physiology
MH  - Pyroglyphidae/*parasitology
EDAT- 2008/03/04 09:00
MHDA- 2008/08/02 09:00
CRDT- 2008/03/04 09:00
PHST- 2008/03/04 09:00 [pubmed]
PHST- 2008/08/02 09:00 [medline]
PHST- 2008/03/04 09:00 [entrez]
AID - 2007-0441OC [pii]
AID - 10.1165/rcmb.2007-0441OC [doi]
PST - ppublish
SO  - Am J Respir Cell Mol Biol. 2008 Jul;39(1):61-7. doi: 10.1165/rcmb.2007-0441OC. 
      Epub 2008 Feb 28.