Remodeling in asthma and chronic obstructive lung disease
P. Jeffery. AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, 164 (10, S):
S28-S38(November 2001)16th Annual Transatlantic Airway Conference (TAC), SAN FRANCISCO, CA, JAN, 2001.
Abstract
Asthma and chronic obstructive lung disease (COPD) are both inflammatory
conditions of the lung associated with structural ``remodeling''
inappropriate to the maintenance of normal lung function. The clinically
observed distinctions between asthma and COPD are reflected by
differences in the remodeling process, the patterns of inflammatory
cells and cytokines, and also the predominant anatomic site at which
these alterations occur. In asthma the epithelium appears to be more
fragile than that of COPD, the epithelial reticular basement membrane
(RBM) is significantly thicker, there is marked enlargement of the mass
of bronchial smooth muscle, and emphysema does not occur in the
asthmatic nonsmoker. In COPD, there is epithelial mucous metaplasia,
airway wall fibrosis, and inflammation associated with loss of
surrounding alveolar attachments to the outer wall of small airways:
bronchiolar smooth muscle is increased also. Emphysema is a feature of
severe COPD: in spite of the destructive process, alveolar wall
thickening and focal fibrosis may be detected. The hypertrophy of
submucosal mucus-secreting glands is similar in extent in asthma and
COPD. The number of bronchial vessels and the area of the wall occupied
by them increase in severe corticosteroid-dependent asthma: it is likely
that these increases also occur in severe COPD as they do in
bronchiectasis. Pulmonary vasculature is remodeled in COPD. In asthma
several of these structural alterations begin early in the disease
process, even in the child. In COPD the changes begin later in life and
the associated inflammatory response differs from that in asthma. The
following synopsis defines and compares the key remodeling processes and
proposes several hypotheses.
Jeffery, PK (Reprint Author), Royal Brompton Hosp, Lung Pathol Unit, Imperial Coll, Sydney St, London SW3 6NP, England..
Royal Brompton Hosp, Lung Pathol Unit, Imperial Coll, London SW3 6NP, England.
web-of-science-categories
Critical Care Medicine; Respiratory System
language
English
journal-iso
Am. J. Respir. Crit. Care Med.
unique-id
ISI:000172833700003
times-cited
318
note
16th Annual Transatlantic Airway Conference (TAC), SAN FRANCISCO, CA, JAN, 2001
%0 Journal Article
%1 jef
%A Jeffery, PK
%C 61 BROADWAY, FL 4, NEW YORK, NY 10006 USA
%D 2001
%I AMER THORACIC SOC
%J AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE
%K asthma remodelling
%N 10, S
%P S28-S38
%T Remodeling in asthma and chronic obstructive lung disease
%V 164
%X Asthma and chronic obstructive lung disease (COPD) are both inflammatory
conditions of the lung associated with structural ``remodeling''
inappropriate to the maintenance of normal lung function. The clinically
observed distinctions between asthma and COPD are reflected by
differences in the remodeling process, the patterns of inflammatory
cells and cytokines, and also the predominant anatomic site at which
these alterations occur. In asthma the epithelium appears to be more
fragile than that of COPD, the epithelial reticular basement membrane
(RBM) is significantly thicker, there is marked enlargement of the mass
of bronchial smooth muscle, and emphysema does not occur in the
asthmatic nonsmoker. In COPD, there is epithelial mucous metaplasia,
airway wall fibrosis, and inflammation associated with loss of
surrounding alveolar attachments to the outer wall of small airways:
bronchiolar smooth muscle is increased also. Emphysema is a feature of
severe COPD: in spite of the destructive process, alveolar wall
thickening and focal fibrosis may be detected. The hypertrophy of
submucosal mucus-secreting glands is similar in extent in asthma and
COPD. The number of bronchial vessels and the area of the wall occupied
by them increase in severe corticosteroid-dependent asthma: it is likely
that these increases also occur in severe COPD as they do in
bronchiectasis. Pulmonary vasculature is remodeled in COPD. In asthma
several of these structural alterations begin early in the disease
process, even in the child. In COPD the changes begin later in life and
the associated inflammatory response differs from that in asthma. The
following synopsis defines and compares the key remodeling processes and
proposes several hypotheses.
@article{jef,
abstract = {{Asthma and chronic obstructive lung disease (COPD) are both inflammatory
conditions of the lung associated with structural ``remodeling{''}
inappropriate to the maintenance of normal lung function. The clinically
observed distinctions between asthma and COPD are reflected by
differences in the remodeling process, the patterns of inflammatory
cells and cytokines, and also the predominant anatomic site at which
these alterations occur. In asthma the epithelium appears to be more
fragile than that of COPD, the epithelial reticular basement membrane
(RBM) is significantly thicker, there is marked enlargement of the mass
of bronchial smooth muscle, and emphysema does not occur in the
asthmatic nonsmoker. In COPD, there is epithelial mucous metaplasia,
airway wall fibrosis, and inflammation associated with loss of
surrounding alveolar attachments to the outer wall of small airways:
bronchiolar smooth muscle is increased also. Emphysema is a feature of
severe COPD: in spite of the destructive process, alveolar wall
thickening and focal fibrosis may be detected. The hypertrophy of
submucosal mucus-secreting glands is similar in extent in asthma and
COPD. The number of bronchial vessels and the area of the wall occupied
by them increase in severe corticosteroid-dependent asthma: it is likely
that these increases also occur in severe COPD as they do in
bronchiectasis. Pulmonary vasculature is remodeled in COPD. In asthma
several of these structural alterations begin early in the disease
process, even in the child. In COPD the changes begin later in life and
the associated inflammatory response differs from that in asthma. The
following synopsis defines and compares the key remodeling processes and
proposes several hypotheses.}},
added-at = {2013-01-07T12:32:46.000+0100},
address = {{61 BROADWAY, FL 4, NEW YORK, NY 10006 USA}},
affiliation = {{Jeffery, PK (Reprint Author), Royal Brompton Hosp, Lung Pathol Unit, Imperial Coll, Sydney St, London SW3 6NP, England..
Royal Brompton Hosp, Lung Pathol Unit, Imperial Coll, London SW3 6NP, England.}},
author = {Jeffery, PK},
author-email = {{p.jeffery@ic.ac.uk}},
biburl = {https://www.bibsonomy.org/bibtex/2f15e4e193d9e5ecffb885b73aed83fab/jehiorns},
doc-delivery-number = {{504AH}},
interhash = {e23ac4e1dd8e9d73761ed68c100b29ca},
intrahash = {f15e4e193d9e5ecffb885b73aed83fab},
issn = {{1073-449X}},
journal = {{AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE}},
journal-iso = {{Am. J. Respir. Crit. Care Med.}},
keywords = {asthma remodelling},
keywords-plus = {{AIRWAY SMOOTH-MUSCLE; GOBLET CELL HYPERPLASIA; PULMONARY-DISEASE;
BRONCHIAL-ASTHMA; BASEMENT-MEMBRANE; SUBEPITHELIAL FIBROSIS; PERIPHERAL
AIRWAYS; STRUCTURAL-CHANGES; FATAL ASTHMA; INFLAMMATION}},
language = {{English}},
month = {{NOV 15}},
note = {{16th Annual Transatlantic Airway Conference (TAC), SAN FRANCISCO, CA, JAN, 2001}},
number = {{10, S}},
number-of-cited-references = {{71}},
pages = {{S28-S38}},
publisher = {{AMER THORACIC SOC}},
research-areas = {{General \& Internal Medicine; Respiratory System}},
researcherid-numbers = {{Mac Sharry, John/B-5509-2011}},
times-cited = {{318}},
timestamp = {2013-01-07T12:32:47.000+0100},
title = {{Remodeling in asthma and chronic obstructive lung disease}},
type = {{Article; Proceedings Paper}},
unique-id = {{ISI:000172833700003}},
volume = {{164}},
web-of-science-categories = {{Critical Care Medicine; Respiratory System}},
year = {{2001}}
}