Collagen and mucopolysaccharide production in growing lung fibroblasts exposed to chrysotile asbestos

Richards, Roy J.; Morris, T. G.

doi:10.1016/0024-3205(73)90332-9

Cited by 38 publications

(9 citation statements)

References 4 publications

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“…This ability of chrysotile to directly cause excessive deposition of collagen appeared confirmed with subsequent studies on different fibroblast strains (1), and parallel investigations showed the toxic effects of this mineral at the light microscopic level, indicating that reticulin deposition in chrysotile-exposed cultures was abnormal (7). Electron microscope studies suggested that chrysotile initiated an early maturation process in fibroblasts, an event which would seem to explain the ability of the mineral to induce excessive collagen deposition in the cultures (4).…”

Section: Introductionmentioning

confidence: 60%

“…Aerosil A380 silica is a finely divided preparation which tends to aggregate in solution although 90% of the aggregates are less than 1 and cell mat hydroxyproline levels in lung fibroblasts over a period of 3 weeks are shown in Figure 2. These studies were repeated with a number of different mineral samples of assumed or unknown fibrogenic potential in vivo, and a summary of the effects of different doses (10-1000 ,g/culture), administered to cultures on day 3, on the levels of DNA and cell mat hydroxyproline assayed 3 weeks later is shown in Figure 3.…”

Section: Mineralsmentioning

confidence: 99%

“…Rabbit lung fibroblasts maintained in vitro over 3 weeks show at least two, and possibly more, phases of development (1,2) (Fig. 1).…”

Section: Introductionmentioning

confidence: 99%

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Reaction of mineral dusts with primary lung fibroblast cultures.

Richards¹,

Hunt²

1983

Environ Health Perspect

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The complex metabolism of rabbit lung fibroblast cultures maintained over 24 days in vitro and their interaction with the fibrogenic group of asbestos minerals is reviewed. The differential effects of nine dusts given as a single dose to 3-day-old fibroblast cultures which were then analyzed for DNA, protein and cell mat hydroxyproline after 3 weeks are discussed.A comparison is made of the ability of these minerals to promote reticulin deposition in vivo following instillation into rats with the ability of each mineral to alter cell mat hydroxyproline levels in fibroblast cultures. Because this comparison is poor for some of the minerals investigated, it is concluded that with the current methodology the fibroblast cultures do not provide an adequate in vitro test system for assessing the potential fibrogenicity of a mineral in vivo.

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Section: Introductionmentioning

confidence: 60%

Section: Mineralsmentioning

confidence: 99%

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Reaction of mineral dusts with primary lung fibroblast cultures.

Richards¹,

Hunt²

1983

Environ Health Perspect

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“…Asbestos, glass, and other fibrous dusts all have been shown to stimulate collagen synthesis (36,37). Fibers over 5 um in length are sometimes incompletely ingested by macrophages (38) and may lead to macrophage death or release of mediators.…”

Section: Macrophage Damage and Pulmonary Connective Tissue: Fibrogenesismentioning

confidence: 99%

“…Rather, the interaction of a particle with a macrophage is thought to release factors which stimulate local production of collagen by fibroblasts. It is unlikely that macrophages differentiate into collagen-synthesizing fibroblasts (42,43) and the addition of silica to cultured fibroblasts does not stimulate collagen biosynthesis or release (37).…”

Section: Macrophage Damage and Pulmonary Connective Tissue: Fibrogenesismentioning

confidence: 99%

Macrophage damage in relation to the pathogenesis of lung diseases.

Brain¹

1980

Environ Health Perspect

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Pulmonary macrophages are important since their migratory patterns and behavior are often pivotal events in the pathogenesis of pulmonary disease. Alveolar macrophages act to decrease the probability of particle penetration through epithelial barriers, and their phagocytic and lytic potentials provide most of the known bactericadal properties of the lung. Macrophages are also involved in immune responses and in defense against neoplasms. Increased inert or infectious particles stimulate the recruitment of additional macrophages. Most free cells containing particles eventually reach the airways and are quickly carried to the pharynx and swallowed. In addition, evidence has now accumulated that macrophages play a part in the pathogenesis of pulmonary diseases. For example, the ingestion of some particles by macrophages causes a release of lysosomal enzymes into the macrophage cytoplasm. These enzymes may kill the macrophage, and dead or dying macrophages release a substance with attracts fibroblasts that elicit fibrogenic responses. Other toxic particles, such as cigarette smoke, my lead to a release of proteases and other toxic enzymes. All particles are capable of competitive inhibition of phagocytosis in macrophages and many may be cytotoxic and further depress phagocytosis. In addition, connective tissue macrophages may contribute to lung disease by concentrating and storing potent carcinogens or other toxic particles close to a reactive bronchial epithelium for long periods. Thus, even through macrophages serve as a first line of defense for the alveolar surface, they may also be capable of injuring the host while exercising their defensive role.

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Macrophages in the Respiratory Tract

Brain

1985

Comprehensive Physiology

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Collagen and mucopolysaccharide production in growing lung fibroblasts exposed to chrysotile asbestos

Cited by 38 publications

References 4 publications

Reaction of mineral dusts with primary lung fibroblast cultures.

Reaction of mineral dusts with primary lung fibroblast cultures.

Macrophage damage in relation to the pathogenesis of lung diseases.

Macrophages in the Respiratory Tract

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