Synergistic inflammatory effect of PM10 with mycotoxin deoxynivalenol on human lung epithelial cells. (15th September 2015)

• Record Type: Journal Article
• Authors: Capasso, Laura; Longhin, Eleonora; Caloni, Francesca; Camatini, Marina; Gualtieri, Maurizio
• Is Part Of: Toxicon. Volume 104(2015)
• Page Start: 65
• Page End: 72
• Publication Date: 2015-09-15
• Subjects: Deoxynivalenol -- Particulate matter -- Human pulmonary cells -- Inflammation -- In vitro; Toxins -- Periodicals; Venom -- Periodicals; 615.9
• DOI: 10.1016/j.toxicon.2015.08.008
• Languages: English
• ISSNs: 0041-0101

Abstract

Abstract: The presence of deoxynivalenol (DON), a mycotoxin produced by Fusarium species, has been reported worldwide in food and feedstuffs. Even though oral intake is the main route of exposure, DON inhalation is also of concern in workers and exposed population. Particulate matter (PM) is one of the most important causes of air quality detriment and it induces several adverse health effects. Therefore it is of primary importance to understand possible combined effects of DON and PM. The alveolar type II, A549, and the bronchial epithelial, BEAS-2B, cell lines were exposed for 24 h to different concentrations of DON (10–1000 ng/ml), PM10 (5 μg/cm 2, sampled in summer or winter season), and a combination of these pollutants. Cell death, interleukins release and cell cycle alteration were analysed; protein array technique was also applied to evaluate proteins activation related to MAP-kinases cascade. Our results demonstrate that low doses of PM and DON used alone have scarce toxic effects, while induce cytotoxicity and inflammation when used in combination. This observation outlines the importance of investigation on the combined effects of air pollutants for their possible outcomes on human health. Highlights: PM and DON are causes of air quality detriment. Low doses of PM and DON determine biological effects in human pulmonary cells. Cell cycle of BEAS-2B was significantly altered by DON exposure. PM and DON in combination trigger synergistic cytotoxic and inflammatory responses. MAPKs pathway activation is sustained in co-exposure condition.