Cellular events in alveolitis and the evolution of pulmonary fibrosis

Burkhardt, A; Cottier, H.

doi:10.1007/bf02890055

Cited by 20 publications

(6 citation statements)

References 108 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The present morphologic study has demonstrated the partial destruction of pneumocytes (especially type I) and the beginning of cubold metaplasia (type II pneumocytes) in alveolitis. Our results confirm the presence of cuboid metaplasia of the alveolar epithelium as a result of severe or repetitive damage to the pulmonary parenchyma, described by other authors [6]. It may be regarded as a distinct sign of preceding type I pneumocyte necrosis, alveolar denudation and subsequent regeneration.…”

Section: Discussionsupporting

confidence: 80%

“…This inflammatory infiltration of the interstitial space is characteristically accompanied by type I pneumocyte damage and type II pneumocyte proliferation. This type of cuboid metaplasia or socalled adenoid transformation of the alveolar epithelium is a prominent feature of alveolitis [6,15,16,18]. A large number of macrophages accumulate in the alveolar lumen.…”

Section: Discussionmentioning

confidence: 99%

“…The accumulated osmiophilic lamellar bodies lead to phagocytosis by macrophages and may contribute to macrophage accumulation. Today there is no doubt that macrophage-derived growth factors stimulate the fibroblasts in the pulmonary interstitium [2,6,7]. The number of fibrocytes and myofibroblasts is increased in the interstitial space, and additional pericapillary pericytes can be observed [1,[3][4][5]17].…”

Section: Discussionmentioning

confidence: 99%

See 2 more Smart Citations

Ultrastructural study on human lung in alveolitis versus pulmonary fibrosis

Fischer

Morgenroth

1993

Clin Investig

View full text Add to dashboard Cite

Lung specimens of 21 patients with diffuse interstitial lung disease were examined. The present ultrastructural study outlines the topography and distribution of inflammatory changes in the interstitium, endothelium, and in pneumocytes and phagocytes. Alveolitis is characterized by marked regenerative activity of type II pneumocytes (cuboid metaplasia), intraluminal macrophage accumulation, endothelial swelling, multilamination of the endothelial basement membrane, pericapillary edema, and primarily by cellular infiltrates in the interstitial space. The most prominent feature of the interstitium in pulmonary fibrosis is the lack of immunoinflammatory cells. In some areas there is a marked absence of alveolar lumen while only a small number of macrophages are present in the remaining alveolar lumen. Most of the capillaries in the fibrous septum have been destroyed. Ultrastructural studies of lung biopsies in patients with diffuse interstitial lung disease allow the differentiation between alveolitis and pulmonary fibrosis and thus contribute to a therapeutic decision.

show abstract

Section: Discussionsupporting

confidence: 80%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Ultrastructural study on human lung in alveolitis versus pulmonary fibrosis

Fischer

Morgenroth

1993

Clin Investig

View full text Add to dashboard Cite

show abstract

“…amounts of extracellular matrix (ECM). Collapsed alveoli thus become sealed with epithelial cells directly appositioned to each other, so-called collapse induration (9,10,45,102). Within the collapsed alveolar walls, abundant basal lamina material without endothelial or epithelial cell contact is present.…”

Section: Diffuse Parenchymal Lung Diseases/pulmonary Fibrosismentioning

confidence: 99%

Quantitative microscopy of the lung: a problem-based approach. Part 2: stereological parameters and study designs in various diseases of the respiratory tract

Mühlfeld

Ochs

2013

American Journal of Physiology-Lung Cellular and Molecular Phys

123

View full text Add to dashboard Cite

Design-based stereology provides efficient methods to obtain valuable quantitative information of the respiratory tract in various diseases. However, the choice of the most relevant parameters in a specific disease setting has to be deduced from the present pathobiological knowledge. Often it is difficult to express the pathological alterations by interpretable parameters in terms of volume, surface area, length, or number. In the second part of this companion review article, we analyze the present pathophysiological knowledge about acute lung injury, diffuse parenchymal lung diseases, emphysema, pulmonary hypertension, and asthma to come up with recommendations for the disease-specific application of stereological principles for obtaining relevant parameters. Worked examples with illustrative images are used to demonstrate the work flow, estimation procedure, and calculation and to facilitate the practical performance of equivalent analyses.

show abstract

“…23 Interestingly, sections of denuded basement membranes in various alveoli appose, become ''stuck'' together, and are incorporated into alveolar septae. 24 In many areas, the entire wall on both sides of the alveolus is involved, and the alveolus completely collapses. An additional histologic feature of this phase is conspicuous microvascular endothelial cell injury, which is accompanied by vascular intimal fibroproliferation, medial hypertrophy, and thrombus in situ.…”

Section: Pathologymentioning

confidence: 99%

Acute Interstitial Pneumonia and Acute Exacerbations of Idiopathic Pulmonary Fibrosis

Swigris¹,

Brown²

2006

Semin Respir Crit Care Med

View full text Add to dashboard Cite

Acute interstitial pneumonia (AIP) and acute exacerbations of idiopathic pulmonary fibrosis (AEIPF) are similar respiratory disorders characterized by the rapid development of progressive dyspnea and cough. Both frequently lead to respiratory failure and death. Pathologically, each is characterized by the presence of a diffuse alveolar damage (DAD) pattern; in AIP, DAD is the sole pattern, whereas in AEIPF DAD is superimposed upon a background usual interstitial pneumonia. They differ in that patients with AEIPF have preexisting idiopathic pulmonary fibrosis, whereas patients with AIP have no predisposing disorders to account for their disease. Because both presentations overlap with multiple other causes of acute lung injury, a comprehensive evaluation is necessary to rule out disorders such as overwhelming infection or congestive heart failure. Although a confident diagnosis can be achieved without it, a surgical lung biopsy is necessary to provide a definitive diagnosis. Despite minimal evidence, glucocorticoids are frequently begun once microbiological evaluation confirms the absence of infection. Despite therapy, the case fatality rate ranges up to 70% for both, with most patients dying in the first 2 weeks. Survivors of the acute event can recover to their previous baseline; however, most AIP survivors will stabilize with some functional impairment, whereas in those with AEIPF, progressive fibrosis with functional deterioration is the rule.

show abstract

Cellular events in alveolitis and the evolution of pulmonary fibrosis

Cited by 20 publications

References 108 publications

Ultrastructural study on human lung in alveolitis versus pulmonary fibrosis

Ultrastructural study on human lung in alveolitis versus pulmonary fibrosis

Quantitative microscopy of the lung: a problem-based approach. Part 2: stereological parameters and study designs in various diseases of the respiratory tract

Acute Interstitial Pneumonia and Acute Exacerbations of Idiopathic Pulmonary Fibrosis

Contact Info

Product

Resources

About