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Research Article

Ferruginous bodies exert a strong proinflammatory effect

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ABSTRACT

One of the main problems related to ferruginous-asbestos bodies (ABs) exposure is their potential pathogenetic role in asbestos-related diseases. The aim of this study was to examine whether purified ABs, might stimulate inflammatory cells. ABs were isolated by exploiting their magnetic properties, therefore avoiding the strong chemical treatment usually employed for this purpose. This latter treatment, which is based upon the digestion of organic matter with concentrated hypochlorite, may markedly modify the AB structure and consequently also their “in vivo” manifestations. ABs were found to induce secretion of human neutrophil granular component myeloperoxidase, as well as stimulate rat mast cell degranulation. Data demonstrated that by triggering secretory processes in inflammatory cells, purified ABs may play a role in the pathogenesis of asbestos-related diseases by continuing and enhancing the pro-inflammatory activity of the asbestos fibers.

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Acknowledgments

The authors are indebted to Elisa Trevisan for her valuable technical contribute.

Disclosure statement

No potential conflict of interest was reported by the author(s).

Data availability statement

The data that support the findings in this paper are available from the corresponding authors [GZ e VB] upon reasonable request.

Supplementary material

Supplemental data for this article can be accessed online at https://doi.org/10.1080/15287394.2023.2181899

Additional information

Funding

This research was funded by grants from: Italian League for the Fight Against Cancer - Associazione provinciale isontina LILT (Lega Italiana Lotta contro i Tumori), Bando Ricerca Sanitaria 2017-programma 5 per mille anno 2015 and Municipality of Monfalcone (Gorizia); Regione Autonoma Friuli-Venezia Giulia, Assessorato alla Salute e Protezione Sociale, LR 22/2001 (decree 1124/SPS, 09/20/2016, No. 1299); We thank Ceric-Eric (Trieste, Italy) for supporting the doctoral fellowship to M.Z.

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