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.
Keywords: Cytoskeleton; Inflammation; Interleukin release; Particulate matter.
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