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Iron oxide nanoparticles (Fe 2 O 3 NPs) is the main component of air pollution particles in urban rail transit environment. People are more exposed to Fe 2 O 3 NPs, however, the studies on relationship between Fe 2 O 3 NPs and respiratory health are limited. In the present study, acute airway inflammation caused by Fe 2 O 3 NPs and its possible mechanism were investigated. BALB/c mice were intratracheally challenged with different concentrations of Fe 2 O 3 NPs. Fe 2 O 3 NPs induced bronchial epithelial barrier function damage, infiltration of neutrophils and lymphocytes into the airway submucosa, secretion of mucus in the airway epithelium and elevated expression of eosinophil major basic protein (EMBP) in lungs. Compared with the control group, Fe 2 O 3 NPs increased eosinophils by 20 times in bronchoalveolar lavage fluid (BALF), and markedly increased eosinophils related cytokines and chemokines, including interleukin (IL) -5, IL-33, thymic stromal lymphopoietin (TSLP), monocyte chemotactic protein (MCP)-3, eotaxin, tumor necrosis factor (TNF)-α, keratinocyte chemoattractant (KC).Furthermore, Fe 2 O 3 NPs up-regulated levels of IL-5, MCP-3, eotaxin, and KC in serum. In vitro studies showed that Fe 2 O 3 NPs increased the genes and proteins expression of Toll-like receptors (TLR)-2, TLR4, TNF receptor associated factor 6 (TRAF6), myeloid differentiation factor 88 (MyD88), nuclear factor (NF)-κB, and TNF-α in RAW267.4 cells. The downstream inflammatory cytokine protein expression and release such as TNF-α was significantly decreased after using TLR2/TLR4 inhibitor OxPAPC, but not MyD88 inhibitor ST2825. These results suggest that TLR2 and TLR4 played important role in Fe 2 O 3 NPs inducing acute eosinophilic airway inflammation in the murine lung.

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