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Milan winter fine particulate matter (wPM2.5) induces IL-6 and IL-8 synthesis in human bronchial BEAS-2B cells, but specifically impairs IL-8 release

TitoloMilan winter fine particulate matter (wPM2.5) induces IL-6 and IL-8 synthesis in human bronchial BEAS-2B cells, but specifically impairs IL-8 release
Tipo di pubblicazioneArticolo su Rivista peer-reviewed
Anno di Pubblicazione2018
AutoriLonghin, E., Holme J.A., Gualtieri Maurizio, Camatini M., and Øvrevik J.
RivistaToxicology in Vitro
Volume52
Paginazione365-373
ISSN08872333
Parole chiaveactin filament, Adsorption, air pollutant, Air Pollutants, article, BEAS-2B cell line, bioaccumulation, cell damage, Cell Line, cell membrane transport, cell vacuole, cellular distribution, Chemical composition, Cities, city, combustion, controlled study, cytokine production, cytokine release, cytoskeleton, Cytotoxicity, fluorescence microscopy, genetics, human, human cell, Humans, IL6 protein, IL8 protein, immunofluorescence microscopy, interleukin 6, interleukin 8, Interleukin-6, Interleukin-8, Italy, lipopolysaccharide, messenger RNA, messenger RNA synthesis, metabolism, particulate matter, protein defect, protein expression, protein localization, season, Seasons, summer, suspended particulate matter, time factor, Toxicity, urban area, winter
Abstract

Inflammatory responses have an important role in the onset of many lung diseases associated with urban airborne particulate matter (PM). Here we investigate effects and mechanisms linked to PM-induced expression and release of two main interleukins, IL-6 and IL-8, in human bronchial epithelial BEAS-2B cells. The cells were exposed to well characterized Milan city PM, winter PM2.5 (wPM2.5) and summer PM10 (sPM10), representing combustion and non-combustion sources, respectively. Both wPM2.5 and sPM10 increased mRNA-synthesis and intracellular protein levels of IL-6 and IL-8. Exposure to sPM10 also resulted in continuous and time-dependent increases in release of IL-6 and IL-8 for up to 48 h. By comparison, in wPM2.5-exposed cells IL-8 release was not significantly augmented, while extracellular IL-6 levels were increased but remained constant beyond 24 h exposure. Moreover, wPM2.5 also reduced the lipopolysaccharide (LPS)-increased release of IL-8. No cytotoxicity or significant adsorption of cytokines to wPM2.5 were observed. Immunofluorescence microscopy revealed an accumulation of IL-8 in intracellular vesicles and alterations in actin filament organization in wPM2.5 exposed cells, suggesting that the trafficking of vesicles carrying interleukins to the plasma membrane might be inhibited. Thus, wPM2.5 appeared to impair cytokine release in BEAS-2B cells, in particular of IL-8, possibly by damaging cytoskeletal function involved in protein secretion. © 2018 Elsevier Ltd

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URLhttps://www.scopus.com/inward/record.uri?eid=2-s2.0-85050389337&doi=10.1016%2fj.tiv.2018.07.016&partnerID=40&md5=2ec6c8a7e8fb473add31548ef044abba
DOI10.1016/j.tiv.2018.07.016
Citation KeyLonghin2018365