Intratracheally administered iron oxide nanoparticles induced murine lung inflammation depending on T cells and B cells.

Iron oxide nanoparticles (Fe2O3 NPs), produced in track traffic system and a wide range of industrial production, poses a great threat to human health. However, there is little research about the mechanism of Fe2O3 NPs toxicity on respiratory system. Rag1-/- mice which lack functional T and B cells were intratracheally challenged with Fe2O3 NPs, and interleukin (IL)-33 as an activator of group 2 innate lymphoid cells (ILC2s) to observe ILC2s changes. The lung inflammatory response to Fe2O3 NPs was alleviated in Rag1-/- mice compared with wild type (WT) mice. Infiltration of inflammatory cells and collagen deposition in tissue, leukocyte numbers (neutrophils, macrophages and lymphocytes), cytokine levels, such as IL-6, IL-13 and thymic stromal lymphopoietin (TSLP), and expression of Toll-like receptor (TLR)2, TLR4, and downstream myeloid differentiation factor (MyD)88, nuclear factor (NF)-κB and tumor necrosis factor (TNF)-α were decreased in lungs. Fe2O3 NPs markedly elevated ILC2s compared with the control, but ILC2s numbers were much lower compared with IL-33 in both WT and Rag1-/- mice. Furthermore, ILC2s amounts were strongly greater in Rag1-/- mice than WT mice. Our results suggested that Fe2O3 NPs induced sub-chronic pulmonary inflammation, which is majorly dependent on T cells and B cells rather than ILC2s.