期刊
INTERNATIONAL JOURNAL OF NANOMEDICINE
卷 7, 期 -, 页码 2729-2737出版社
DOVE MEDICAL PRESS LTD
DOI: 10.2147/IJN.S31054
关键词
iron oxide nanoparticle; T cell; macrophage; delayed-type hypersensitivity
资金
- National Science Council, Executive Yuan (Taipei, Taiwan) [NSC98-2320-B-002-036-MY3, NSC99-2313-B264-001-MY3]
- Kaohsiung Medical University Research Foundation (Kaohsiung City, Taiwan) [KMU-ER013]
Background: It was recently reported that iron oxide nanoparticles attenuated antigen-specific humoral responses and T cell cytokine expression in ovalbumin-sensitized mice. It is presently unclear whether iron oxide nanoparticles influence T helper 1 cell-mediated immunity. The present study aimed to investigate the effect of iron oxide nanoparticles on delayed-type hypersensitivity (DTH), whose pathophysiology requires the participation of T helper 1 cells and macrophages. Methods: DTH was elicited by a subcutaneous challenge with ovalbumin to the footpads of mice sensitized with ovalbumin. Iron oxide nanoparticles (0.2-10 mg iron/kg) were administered intravenously 1 hour prior to ovalbumin sensitization. Local inflammatory responses were examined by footpad swelling and histological analysis. The expression of cytokines by splenocytes was measured by enzyme-linked immunosorbent assay. Results: Administration of iron oxide nanoparticles, in a dose-dependent fashion, significantly attenuated inflammatory reactions associated with DTH, including the footpad swelling, the infiltration of T cells and macrophages, and the expression of interferon-gamma, interleukin-6, and tumor necrosis factor-a in the inflammatory site. Iron oxide nanoparticles also demonstrated a suppressive effect on ovalbumin-stimulated production of interferon-gamma by splenocytes and the phagocytic activity of splenic CD11b(+) cells. Conclusion: These results demonstrated that a single dose of iron oxide nanoparticles attenuated DTH reactions by suppressing the infiltration and functional activity of T helper 1 cells and macrophages in response to antigen stimulation.
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