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Differential protein folding and chemical changes in lung tissues exposed to asbestos or particulates.

Pascolo L, Borelli V, Canzonieri V, Gianoncelli A, Birarda G, Bedolla DE, Salomé M, Vaccari L, Calligaro C, Cotte M, Hesse B, Luisi F, Zabucchi G, Melato M, Rizzardi C - Sci Rep (2015)

Bottom Line: Both asbestos and particulates alter lung iron homeostasis, with a more marked effect in asbestos exposure. μFTIR analyses revealed abundant proteins on asbestos bodies but not on anthracotic particles.Most importantly, the analyses demonstrated that the asbestos coating proteins contain high levels of β-sheet structures.The occurrence of conformational changes in the proteic component of the asbestos coating provides new insights into long-term asbestos effects.

View Article: PubMed Central - PubMed

Affiliation: Institute for Maternal and Child Health, IRCCS Burlo Garofolo, Trieste, Italy.

ABSTRACT
Environmental and occupational inhalants may induce a large number of pulmonary diseases, with asbestos exposure being the most risky. The mechanisms are clearly related to chemical composition and physical and surface properties of materials. A combination of X-ray fluorescence (μXRF) and Fourier Transform InfraRed (μFTIR) microscopy was used to chemically characterize and compare asbestos bodies versus environmental particulates (anthracosis) in lung tissues from asbestos exposed and control patients. μXRF analyses revealed heterogeneously aggregated particles in the anthracotic structures, containing mainly Si, K, Al and Fe. Both asbestos and particulates alter lung iron homeostasis, with a more marked effect in asbestos exposure. μFTIR analyses revealed abundant proteins on asbestos bodies but not on anthracotic particles. Most importantly, the analyses demonstrated that the asbestos coating proteins contain high levels of β-sheet structures. The occurrence of conformational changes in the proteic component of the asbestos coating provides new insights into long-term asbestos effects.

No MeSH data available.


Related in: MedlinePlus

Histological images of asbestosis and anthracosis.Panel A, B, C and D are micrographs from the histological sections used in the study, coloured with Perls’ staining. Panel A (20x) shows asbestos bodies and anthracotic material embedded within asbestosis tissue. Panel B (40x), asbestos bodies strongly Perls’ positive (higher magnification of Panel A). Panel C (40x), carbonaceous particles in a patient with anthracosis (higher magnification of Panel A). Panel D, Perls’ signal in proximity of anthracosis in a patient unexposed to asbestos.
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f1: Histological images of asbestosis and anthracosis.Panel A, B, C and D are micrographs from the histological sections used in the study, coloured with Perls’ staining. Panel A (20x) shows asbestos bodies and anthracotic material embedded within asbestosis tissue. Panel B (40x), asbestos bodies strongly Perls’ positive (higher magnification of Panel A). Panel C (40x), carbonaceous particles in a patient with anthracosis (higher magnification of Panel A). Panel D, Perls’ signal in proximity of anthracosis in a patient unexposed to asbestos.

Mentions: The patients with asbestosis had medium to high content of asbestos bodies in their pulmonary parenchyma, according to asbestos bodies counts performed on digested lung tissue (as reported in Table 1). We selected for the present analyses comparable lung tissue sections, having the specific histological features of asbestosis and clearly recognizable asbestos bodies. In the selected tissue slices (at least 2 per patient), the examined asbestos bodies were of various dimensions and shapes. Some of them were isolated or grouped inside dense interstitial fibrosis deposition material, others were surrounded and/or interacting with macrophages and giant cells. On many occasions, asbestos bodies were found surrounded by black pigmented material. In fact, these two types of pollutants tend to accumulate in similar regions. In the cases of only anthracosis, included in the present study, particles were concentrated around bronchovascular bundles, in interlobular septa, and beneath the pleura, being in relation to lymphatic vessel network. Dust material is dispersed, and relatively inert, causing little or no fibrosis. Only in one case is there a zonal fibrosis involving also some adjacent lymph nodes. No examples of massive fibrosis due to fibrogenic particles, which may present either as ‘coal nodules’ (of little functional significance) or as progressive massive fibrosis (which results in pulmonary function abnormalities (coal worker’s pneumoconiosis) were observed in our limited series. Figure 1 shows asbestos bodies compared to anthracosis after staining with the Perls’ Prussian blue method that highlights iron in the ferric state. In panel A, collections of asbestos bodies, other ferruginous bodies and deposits of carbon embedded within fibrous tissue in a case of severe pulmonary asbestosis are observed (20x). As seen in panel B at higher magnification (40x), asbestos bodies are strongly Perls positive due to the ferric iron present in their coating. Moreover, an obvious lighter blue halo surrounding the bodies is observed. In panel C, carbonaceous particles in a patient with anthracosis are shown (40x) as a collection of black granules, widely distributed in the fibrous tissue. It is generally accepted that anthracotic deposits are negative for iron stains, but in Fig. 1(D) the presence of a weakly blue stained thin outline, similar to that seen around asbestos bodies is easily observed. Panel D shows some macrophages floating in the lumen of a subpleural blood vessel of another patient with anthracosis: in the cytoplasm of one of them, indicated by arrows, black granules of coal-pigment-like material are observed along with Perls positive iron deposits (63x). Similar levels of faint positivity have been found in few macrophages and around carbon-like pigmented structures in all the tissues derived from patients presenting anthracosis.


Differential protein folding and chemical changes in lung tissues exposed to asbestos or particulates.

Pascolo L, Borelli V, Canzonieri V, Gianoncelli A, Birarda G, Bedolla DE, Salomé M, Vaccari L, Calligaro C, Cotte M, Hesse B, Luisi F, Zabucchi G, Melato M, Rizzardi C - Sci Rep (2015)

Histological images of asbestosis and anthracosis.Panel A, B, C and D are micrographs from the histological sections used in the study, coloured with Perls’ staining. Panel A (20x) shows asbestos bodies and anthracotic material embedded within asbestosis tissue. Panel B (40x), asbestos bodies strongly Perls’ positive (higher magnification of Panel A). Panel C (40x), carbonaceous particles in a patient with anthracosis (higher magnification of Panel A). Panel D, Perls’ signal in proximity of anthracosis in a patient unexposed to asbestos.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4498377&req=5

f1: Histological images of asbestosis and anthracosis.Panel A, B, C and D are micrographs from the histological sections used in the study, coloured with Perls’ staining. Panel A (20x) shows asbestos bodies and anthracotic material embedded within asbestosis tissue. Panel B (40x), asbestos bodies strongly Perls’ positive (higher magnification of Panel A). Panel C (40x), carbonaceous particles in a patient with anthracosis (higher magnification of Panel A). Panel D, Perls’ signal in proximity of anthracosis in a patient unexposed to asbestos.
Mentions: The patients with asbestosis had medium to high content of asbestos bodies in their pulmonary parenchyma, according to asbestos bodies counts performed on digested lung tissue (as reported in Table 1). We selected for the present analyses comparable lung tissue sections, having the specific histological features of asbestosis and clearly recognizable asbestos bodies. In the selected tissue slices (at least 2 per patient), the examined asbestos bodies were of various dimensions and shapes. Some of them were isolated or grouped inside dense interstitial fibrosis deposition material, others were surrounded and/or interacting with macrophages and giant cells. On many occasions, asbestos bodies were found surrounded by black pigmented material. In fact, these two types of pollutants tend to accumulate in similar regions. In the cases of only anthracosis, included in the present study, particles were concentrated around bronchovascular bundles, in interlobular septa, and beneath the pleura, being in relation to lymphatic vessel network. Dust material is dispersed, and relatively inert, causing little or no fibrosis. Only in one case is there a zonal fibrosis involving also some adjacent lymph nodes. No examples of massive fibrosis due to fibrogenic particles, which may present either as ‘coal nodules’ (of little functional significance) or as progressive massive fibrosis (which results in pulmonary function abnormalities (coal worker’s pneumoconiosis) were observed in our limited series. Figure 1 shows asbestos bodies compared to anthracosis after staining with the Perls’ Prussian blue method that highlights iron in the ferric state. In panel A, collections of asbestos bodies, other ferruginous bodies and deposits of carbon embedded within fibrous tissue in a case of severe pulmonary asbestosis are observed (20x). As seen in panel B at higher magnification (40x), asbestos bodies are strongly Perls positive due to the ferric iron present in their coating. Moreover, an obvious lighter blue halo surrounding the bodies is observed. In panel C, carbonaceous particles in a patient with anthracosis are shown (40x) as a collection of black granules, widely distributed in the fibrous tissue. It is generally accepted that anthracotic deposits are negative for iron stains, but in Fig. 1(D) the presence of a weakly blue stained thin outline, similar to that seen around asbestos bodies is easily observed. Panel D shows some macrophages floating in the lumen of a subpleural blood vessel of another patient with anthracosis: in the cytoplasm of one of them, indicated by arrows, black granules of coal-pigment-like material are observed along with Perls positive iron deposits (63x). Similar levels of faint positivity have been found in few macrophages and around carbon-like pigmented structures in all the tissues derived from patients presenting anthracosis.

Bottom Line: Both asbestos and particulates alter lung iron homeostasis, with a more marked effect in asbestos exposure. μFTIR analyses revealed abundant proteins on asbestos bodies but not on anthracotic particles.Most importantly, the analyses demonstrated that the asbestos coating proteins contain high levels of β-sheet structures.The occurrence of conformational changes in the proteic component of the asbestos coating provides new insights into long-term asbestos effects.

View Article: PubMed Central - PubMed

Affiliation: Institute for Maternal and Child Health, IRCCS Burlo Garofolo, Trieste, Italy.

ABSTRACT
Environmental and occupational inhalants may induce a large number of pulmonary diseases, with asbestos exposure being the most risky. The mechanisms are clearly related to chemical composition and physical and surface properties of materials. A combination of X-ray fluorescence (μXRF) and Fourier Transform InfraRed (μFTIR) microscopy was used to chemically characterize and compare asbestos bodies versus environmental particulates (anthracosis) in lung tissues from asbestos exposed and control patients. μXRF analyses revealed heterogeneously aggregated particles in the anthracotic structures, containing mainly Si, K, Al and Fe. Both asbestos and particulates alter lung iron homeostasis, with a more marked effect in asbestos exposure. μFTIR analyses revealed abundant proteins on asbestos bodies but not on anthracotic particles. Most importantly, the analyses demonstrated that the asbestos coating proteins contain high levels of β-sheet structures. The occurrence of conformational changes in the proteic component of the asbestos coating provides new insights into long-term asbestos effects.

No MeSH data available.


Related in: MedlinePlus