Bronchoalveolar and Lung Tissue Analyses in Asbestos-exposed Humans and Sheep

Bégin, Raymond; Massé, S.; Rola‐Pleszczynski, Marek; Drapeau, Guy; Péloquin, S.; Geoffrey, M.; Labbe, J.; Gouin, S.; Desmarais, Y.; Martel, Marc

doi:10.1007/978-3-642-70630-1_45

Cited by 12 publications

(5 citation statements)

References 14 publications

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“…These were confirmed by another study [86]. In our experimental studies in the sheep model we have fully reported similar evidence of activated macrophages producing excessive amounts of fibronectin, fibroblast growth factor, and neutrophil chemotactic factors, and we have also reported the multifaceted action of asbestos on local and systemic immune lymphocyte responses [21,33,42,66,67,152].…”

Section: Asbestos-exposed Workerssupporting

confidence: 83%

“…In addition, enhanced local proliferation of the in situ macrophage population may a lso contribute to the accumula tion of the mononuclear phagocytes [65]. Thus lungs c hronicaiJy exposed to mineral dusts have an excessive early accumulation of macrophagcs in the lower respiratory tracL, which can be recognized at lung biopsy [5,66] or lung lavage [6,67,68].…”

Section: Lung Tissue Reactionsmentioning

confidence: 99%

“…Following our initial report on a substantial number of long term workers with abnormal 67 Ga scans in the absence of other criteria for asbestosis [5], we investigated several asbestos workers [6][7][8]66] and similar studies were conducted by the National Institute of Health [65,68]. In the studies of RoM et al [65,68] and in our own [6][7][8]66], it was documented that macrophages of the bronchoalveolar space of asbestos exposed workers demonstrated marked structural changes, were producing excessive amounts of fibronectin, fibroblast growth factor, and increased "f-interferon, which could participate in the pathogenesis of asbestosis. These were confirmed by another study [86].…”

Section: Asbestos-exposed Workersmentioning

confidence: 99%

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Recent advances in the pathogenesis and clinical assessment of mineral dust pneumoconioses: asbestosis, silicosis and coal pneumoconiosis

Begin¹,

Cantin²,

Masse³

1989

Eur Respir J

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Recent investigations of the fundamental mechanisms of the mineral dust diseases have substantially increased our understanding of the pathogenesis of the pneumoconioses. In all the mineral dust pneumoconioses, the initial early lung lesion is a fibrosing macrophagic alveolitis. The additional contribution of other lung cell populations is currently under investigation and may identify specific processes for each of the pneumoconioses. Clinical investigations have also progressed with new tools such as Gallium-67 lung scanning, bronchoalveolar lavage analyses, and CT scanning of the thorax; their established values are reviewed in this paper, and areas where progress is needed are considered. The clinical progress in the mineral dust diseases is clearly linked to the basic understanding of the mechanisms of these diseases.

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Section: Asbestos-exposed Workerssupporting

confidence: 83%

Section: Lung Tissue Reactionsmentioning

confidence: 99%

Section: Asbestos-exposed Workersmentioning

confidence: 99%

See 1 more Smart Citation

Recent advances in the pathogenesis and clinical assessment of mineral dust pneumoconioses: asbestosis, silicosis and coal pneumoconiosis

Begin¹,

Cantin²,

Masse³

1989

Eur Respir J

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“…Our study is also of interest as it further characterized the early stage of asbestosis at the time of initial radiographic recognition of the disease process. Previous studies in humans (4,(40)(41)(42) and in several animal models, including sheep [22][23][24][25][26][27][43][44][45][46][47][48][49][50][51][52] have clearly documented that lungs chronically exposed to asbestos or other mineral dusts have an excessive early accumulation of macrophages in the lower respiratory tract.…”

Section: Discussionmentioning

confidence: 99%

Chrysotile asbestos exposures can produce an alveolitis with limited fibrosing activity in a subset of high fibre retainer sheep

Bégin

Cantin²,

Sébastien³

1990

Eur Respir J

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Inhalation of fibrogenic mineral dust may enhance fibronectin (Fn) production by alveolar macrophages and increase fibroblast growth activity (FGA) in lung lavage fluid. To investigate the relationship of these changes to fibre retention and the development of asbestosis, we exposed 15 sheep to 100 mg Canadian chrysotile fibres in 100 ml saline, and ten sheep to 100 ml saline only, at ten day intervals. The animals were studied at 3 month intervals. At month 18, ten sheep had abnormal chest radiograph (category greater than or equal to 1) (group B) and five had normal radiograph (category 0) (group A). Pulmonary function data indicated restrictive patterns of abnormalities in both groups, more severe in group B. Sheep in group A had bronchoalveolar lavage (BAL) cellularity and biochemistry comparable to controls; sheep in group B had significant increases in total BAL cells (x2), macrophages (x2), neutrophils (x4) and eosinophils (x3), increased BAL lactate dehydrogenase and Fn, but FGA and procollagen 3 comparable to controls. Fibre retention was significantly increased in all exposed sheep and 2.5 x higher in group B vs group A despite similar exposures (70 intratracheal, 100 mg chrysotile infusions). Enhanced fibre retention in group B preceded the appearance of disease. This study confirms our earlier observation linking individual susceptibility to development of alveolitis to individual dust burden and provides evidence that the excess of fibre retention can be observed before detectable disease. In addition, we report a chrysotile-induced early alveolitis with incompletely expressed fibrosing activity at the time of initial radiographic detection. The intensity of the alveolitis is related to the degree of fibre retention.

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“…Current understanding of the biologic mechanisms of interstitial lung disease suggests that fibrosis of the lung is the end-stage result of a chronic inflammatory process in the alveoli and the interstitium. 1 In our recent investigations of asbestosexposed humans and sheep, [2][3][4][5][6][7][8][9][10][11][12][13][14][15][16][17] we have reported an inflammatory process in the alveoli and interstitium that preceded the development of interstitial fibrosis. In addition to being documented on lung biopsy materials ( Fig.…”

mentioning

confidence: 99%

Assessment of Disease Activity by Gallium-67 Scan and Lung Lavage in the Pneumoconioses

Bégin¹,

Bisson²,

Boileau³

et al. 1986

Semin Respir Crit Care Med

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Bronchoalveolar and Lung Tissue Analyses in Asbestos-exposed Humans and Sheep

Cited by 12 publications

References 14 publications

Recent advances in the pathogenesis and clinical assessment of mineral dust pneumoconioses: asbestosis, silicosis and coal pneumoconiosis

Recent advances in the pathogenesis and clinical assessment of mineral dust pneumoconioses: asbestosis, silicosis and coal pneumoconiosis

Chrysotile asbestos exposures can produce an alveolitis with limited fibrosing activity in a subset of high fibre retainer sheep

Assessment of Disease Activity by Gallium-67 Scan and Lung Lavage in the Pneumoconioses

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