Nanoparticles are increasingly used in various fields, including biomedicine and electronics. Their size and physical characteristics allow them to easily access the cytosol of tissue or immune cells. Although inorganic metal oxide nano-TiO2 is believed to be biologically inert, an emerging literature reports increased incidence of respiratory diseases in exposed people. Here, we show that instillation of nano-TiO2 induces lung inflammation which is strongly suppressed in IL-1R- and IL-1α-deficient mice. They have drastically reduced neutrophil recruitments in the alveolar space, together with lung inflammatory cytokine productions. Surprisingly, the NLRP3 inflammasome complex seems to be only partially involved. Nlrp3-, ASC- or Casp-1-deficient mice show only a slight reduction in pulmonary inflammatory response. IL-1β-deficient mice exhibit decreased inflammation parameters that are less pronounced than IL-1α-deficient mice. In vitro experiments show that primary pulmonary epithelial cells cultured in presence of nano-TiO2 are able to produce KC and IL-1α, but not IL-1β, to initiate inflammation. In conclusion, it appears that nanoparticles-mediated inflammation is highly dependent on IL-1α and to a less extend on the NLRP3 inflammasome/IL-1β axis. Collectively, these data demonstrate that the expending use of nano-TiO2, e.g. in cosmetics, may present a health hazard and should be taken under consideration, a situation reminiscent of inflammation provoked by asbestos exposure.
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