Lung Structural Changes in Chronic Obstructive Pulmonary Diseases

Davidson, Warren; Bai, Tony R.

doi:10.2174/156801005774912842

Cited by 16 publications

(6 citation statements)

References 27 publications

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“…The role of elastin destruction in the pathogenesis of emphysema is well known (Davidson and Bai, 2005), but there appears to be little discussion about the consequences of leukocyte-mediated elastase-induced degradation of elastin in the major airways. The abundance of elastin we observed in the tracheobronchial tree, even in elderly cadavers, suggests that this deserves further study.…”

Section: Discussion Elastic Fibers In the Trachea And Bronchimentioning

confidence: 99%

Novel insights into the elastic and muscular components of the human trachea

2009

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Despite its probable importance in health and disease, the elastic tissue in the trachea has rarely been investigated. In addition, various aspects of the trachealis muscle are controversial. The aim of this study was to clarify this clinically relevant anatomy. Ten cadaveric tracheobronchial specimens (age range 68-101 years; seven males; no major airway pathology) were qualitatively investigated by microdissection. Serial histologic sections from multiple sites in three specimens were analyzed after staining for elastin. Findings were correlated with observations from video tracheobronchoscopies. An extensive and prominent meshwork of elastic tissue was found within the trachea and bronchi. Elastic fibers were predominantly longitudinal and aggregated into discrete bundles within the membranous wall of the trachea and main bronchi; a discrete fibroelastic membrane bridging the membranous wall of the trachea; and vertical laminae connecting the ends of successive cartilages. The longitudinal elastic bundles continued into the segmental bronchi, becoming thinner and more circumferentially distributed. Trachealis consisted of a transverse layer of smooth muscle deep to the fibroelastic membrane of the membranous wall of the trachea, together with scattered longitudinal muscle bundles, mostly embedded within the fibroelastic membrane in the distal half of the trachea. In conclusion, there is an extensive but relatively neglected elastic framework within the tracheobronchial tree. This is likely to have major clinical relevance to the pathophysiology of respiratory disease and ageing. The trachealis muscle is more complex than previously stated.

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Section: Discussion Elastic Fibers In the Trachea And Bronchimentioning

confidence: 99%

Novel insights into the elastic and muscular components of the human trachea

2009

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“…Yet, the remodeling of the lung vasculature can be profound and persistent, as exemplified in a variety of non-allergic diseases like pulmonary arterial hypertension (PAH), idiopathic PAH [9, 10], chronic obstructive pulmonary disease [11,12,13], systemic sclerosis and systemic lupus erythematosus [9, 14, 15]. The changes in these conditions range from increased endothelial proliferation, intimal fibrosis, increased medial thickness, luminal occlusion and plexiform lesions [9, 13, 14, 16, 17]. The importance of inflammation and inflammatory processes in the pathogenesis was recently highlighted [18, 19], and previous findings of vascular remodeling induced by allergic airway inflammation [20,21,22] further support this notion.…”

Section: Introductionmentioning

confidence: 99%

Allergic Airway Inflammation Initiates Long-Term Vascular Remodeling of the Pulmonary Circulation

Rydell‐Törmänen¹,

Uller²,

Erjefält³

2009

Int Arch Allergy Immunol

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Background: Asthma and allergic airway inflammation are associated with persistent structural alterations in the bronchi, i.e. airway remodeling. Previous studies have shown that during allergic airway inflammation, similar structural alterations may also be evoked in the pulmonary circulation. However, it remained unknown whether remodeling of the pulmonary circulation is as persistent as airway remodeling. The aim of this study is to investigate the reversibility and resolution of vascular remodeling, induced by allergic airway inflammation. Methods: A validated mouse model of allergic airway inflammation, utilizing ovalbumin as allergen, was employed. Animals were sacrificed 1 day, 1 week or 1 month after the last allergen exposure, and different parameters of remodeling (smooth muscle mass, proliferation of smooth muscle cells and endothelial cells as well as number of myofibroblasts and procollagen-I-producing cells) were investigated and quantified histologically. Results: Allergen exposure resulted in allergic airway inflammation characterized by a transient leukocyte infiltration and in structural alterations in both airway and vascular compartments. The increase in vascular smooth muscle mass and endothelial proliferation persisted at 1 month after the last allergen exposure. The other parameters and cellular inflammatory response returned to baseline within 1 month after the last allergen challenge. Conclusions: Based on the findings in this study, we conclude that acute allergic airway inflammation, although being initiated from the airways, is able to evoke similar long-term structural alterations in pulmonary vessels as described for bronchi.

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“…In the current literature there are only a few descriptions of pulmonary vascular remodeling following allergic airway inflammation. By contrast, remodeling of these vessels is an accepted feature of several other diseases such as systemic scleroderma [ 8 ], idiopathic pulmonary fibrosis [ 9 ] and COPD [ 10 , 11 ]. The mechanism behind vascular remodeling may vary with disease, but the histological appearances appear to be similar in nature [ 12 ].…”

Section: Introductionmentioning

confidence: 99%