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

Iron oxide nanoparticles (FeO 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 FeO NPs toxicity on respiratory system. Rag1 mice which lack functional T and B cells were intratracheally challenged with FeO NPs, and interleukin (IL)-33 as an activator of group 2 innate lymphoid cells (ILC2s) to observe ILC2s changes. The lung inflammatory response to FeO 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. FeO 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 FeO NPs induced sub-chronic pulmonary inflammation, which is majorly dependent on T cells and B cells rather than ILC2s.