Phagocytic potential of pulmonary alveolar epithelium with particular reference to surfactant metabolism

Corrin, B.

doi:10.1136/thx.25.1.110

Cited by 38 publications

(29 citation statements)

References 12 publications

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“…The air side of the alveolar wall is made up by type I and type II pneumocytes [9,18,36]. Because endocytosis is a cellular function exerted by type I but not by type II pneumocytes [6,7], our finding probably corresponds to particles engulfed by type I pneumocytes; according to Weiss [37] these ingested particles may be conveyed to the interstitium from the alveolar lumen by a vesicular transport.…”

Section: Discussionmentioning

confidence: 89%

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Inflammatory response of the lung to tungsten particles: An experimental study in mice submitted to intratracheal instillation of a calcium tungstate powder

Peao

Águas

et al. 1993

Lung

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Tungsten has been implicated as a cause of a severe form of pneumoconiosis in humans, the so-called "hard metal" lung disease. We have investigated the effect of intratracheal instillation of a powder of calcium tungstate on the pulmonary tissue of CD-1 mice. The tungsten-induced alterations were studied using 3 microanatomical methods: cytologic study of exudates obtained by bronchoalveolar lavage (BAL); histologic examination of paraffin-embedded sections of the lung; and scanning electron microscopic (SEM) examination of lung samples using x-ray microanalysis to detect tungsten in situ. The animals were sacrificed 1, 3, 7, 14 and 21 days after a single intratracheal instillation of 250 micrograms calcium tungstate particles suspended in 100 microliters of saline. We found that the metal particles induced a marked inflammatory response in the bronchoalveolar space characterized by a biphasic attraction of leukocytes with cellular peaks observed at day 1 and 14. More than 50% of the BAL macrophages showed ingested tungsten. In the lung parenchyma, the inflammatory infiltrates were predominantly located at the periphery of the bronchiolar walls. From 7 days on after the tungsten deposition, large inflammatory exudates were seen invading focal areas of the alveolar domain of the lung. SEM views revealed that the tungsten particles could be inside alveolar macrophages, in cells making up the alveolar wall, or inside periacinar lymphatics. Our data document that tungsten particles cause a marked inflammatory response in the lung tissue and that the leukocyte exudates may invade alveolar areas of the lung.(ABSTRACT TRUNCATED AT 250 WORDS)

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Section: Discussionmentioning

confidence: 89%

“…The tungsten salt was chosen because this metal is currently extracted in mines in Portugal and elsewhere, and also because particles from tungsten alloys have been implicated in a particular type of pneumoconiosis, the so-called "hard metal lung disease" [7]. This disorder is often manifested by interstitial lung fibrosis [15,21].…”

Section: Discussionmentioning

confidence: 99%

Inflammatory response of the lung to tungsten particles: An experimental study in mice submitted to intratracheal instillation of a calcium tungstate powder

Peao

Águas

et al. 1993

Lung

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“…It has been assumed that this function is also performed by the type II cell of the alveolar epithelium. Occasional early observations suggested that this was indeed the case (4,5). More recent observations which indicate that type II cells recycle pulmonary surfactant, a material that they synthesize, have prompted renewed interest in endocytic mechanisms in type II cells and in the pathways taken by materials ingested by these cells.…”

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confidence: 99%

Endocytosis in alveolar type II cells: effect of charge and size of tracers.

Williams¹

1984

Proc. Natl. Acad. Sci. U.S.A.

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The type II cell of the alveolar epithelium of adult rats has been studied by electron microscopy to determine its ability to endocytose electron-dense tracers of differing molecular charge and size. The tracers studied were native (anionic) ferritin, cationic ferritin, 70-kilodalton dextran, and colloidal carbon. Alveolar macrophages ingested all tracers in large amounts, while type II cells took up significant amounts of cationic ferritin only. This tracer was observed, in sequence, within small pinocytic vesicles, large electron-lucent multivesicular bodies, small electron-dense multivesicular bodies, and, by 30 min after instillation, within the nonlamellar matrix of lamellar bodies. By 2 hr all lamellar bodies in any labeled cell contained cationic ferritin. Cationic ferritin also appeared to be transported from alveoli to interstitium by vesicles of type II, but not type I, cells. Native ferritin and dextran were observed in the same organelles as cationic ferritin but in much smaller amounts; colloidal carbon was not taken up by type II cells. These tracers were not observed in the alveolar interstitium. Type II cells therefore appear to internalize preferentially the tracer that binds to the cell membrane. Once within the cell, the tracer may enter a pathway that terminates in a lamellar body or, in the case of cationic ferritin, may be ferried across the cell.Results of many studies suggest that the ability to ingest materials by endocytosis is a property shared by most, if not all, cells. The general characteristics of the several types of endocytosis have been reviewed recently by several groups (1-3). It has been assumed that this function is also performed by the type II cell of the alveolar epithelium. Occasional early observations suggested that this was indeed the case (4, 5). More recent observations which indicate that type II cells recycle pulmonary surfactant, a material that they synthesize, have prompted renewed interest in endocytic mechanisms in type II cells and in the pathways taken by materials ingested by these cells. On the basis of the observed rates of clearance from alveoli of several surfactant-associated phospholipids, Hallman et al. (6) proposed that recycling of surfactant may take place by means of a process of bulk uptake. If this were true, it might be expected that a vesicle-mediated pathway would link alveoli with lamellar bodies, the intracellular storage granules of surfactant.This study was therefore undertaken to define the fate of various tracer molecules placed in small quantities in alveoli of intact animals in order to determine how the molecular charge and size of the tracers influenced the uptake, if any, by alveolar epithelial cells and, second, to characterize the intracellular pathways taken by the tracers after uptake. Studies of a similar nature have been carried out to determine the fate of several lectins, one of which binds specifically to the apical plasma membrane of type II cells. These results will be reported later.The observations of these ...

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“…Interestingly, also the other non-tubular material, GNF, shows similar pattern in all three cell types. Moreover, poor ability of both type I and II epithelial cells to uptake carbon black particles has already been described in vivo (Corrin, 1970).…”

Section: Comparison Of Cnms Moamentioning

confidence: 97%

Multi-omics analysis of ten carbon nanomaterials effects highlights cell type specific patterns of molecular regulation and adaptation

et al. 2018

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New strategies to characterize the effects of engineered nanomaterials (ENMs) based on omics technologies are emerging. However, given the intricate interplay of multiple regulatory layers, the study of a single molecular species in exposed biological systems might not allow the needed granularity to successfully identify the pathways of toxicity (PoT) and, hence, portraying adverse outcome pathways (AOPs). Moreover, the intrinsic diversity of different cell types composing the exposed organs and tissues in living organisms poses a problem when transferring in vivo experimentation into cell-based in vitro systems.To overcome these limitations, we have profiled genome-wide DNA methylation, mRNA and microRNA expression in three human cell lines representative of relevant cell types of the respiratory system, A549, BEAS-2B and THP-1, exposed to a low dose of ten carbon nanomaterials (CNMs) for 48 h. We applied advanced data integration and modelling techniques in order to build comprehensive regulatory and functional maps of the CNM effects in each cell type.We observed that different cell types respond differently to the same CNM exposure even at concentrations exerting similar phenotypic effects. Furthermore, we linked patterns of genomic and epigenomic regulation to intrinsic properties of CNM. Interestingly, DNA methylation and microRNA expression only partially explain the mechanism of action (MOA) of CNMs. Taken together, our results strongly support the implementation of approaches based on multi-omics screenings on multiple tissues/cell types, along with systems biology-based multi-variate data modelling, in order to build more accurate AOPs.

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Phagocytic potential of pulmonary alveolar epithelium with particular reference to surfactant metabolism

Cited by 38 publications

References 12 publications

Inflammatory response of the lung to tungsten particles: An experimental study in mice submitted to intratracheal instillation of a calcium tungstate powder

Inflammatory response of the lung to tungsten particles: An experimental study in mice submitted to intratracheal instillation of a calcium tungstate powder

Endocytosis in alveolar type II cells: effect of charge and size of tracers.

Multi-omics analysis of ten carbon nanomaterials effects highlights cell type specific patterns of molecular regulation and adaptation

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