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Iron oxide nanoparticles induce cytokine secretion in a complement-dependent manner in a human whole blood model

May 23, 2017

Highlights:
    • The IONPs activated complement, as measured by C3a, C5a and sC5b-9, and induced the production of pro-inflammatory cytokines in a particle-dose dependent manner, with the strongest response at 10 µg/mL IONPs. Complement inhibitors at C3 (compstatin analog Cp40) and C5 (eculizumab) levels completely inhibited complement activation and secretion of inflammatory mediators induced by the IONPs.
    • Blockade of complement receptors C3aR and C5aR1 significantly reduced the levels of various cytokines, indicating that the particle-induced secretion of inflammatory mediators is mainly C5a and C3a mediated.
    • The IONPs did not induce cell death or reactive oxygen species, which further suggests that complement activation alone was responsible for most of the particle-induced cytokines.
    • Conclusion: These data suggest that the lepirudin anti-coagulated human whole blood model is a valuable ex vivo system to study the inflammatory potential of IONPs. We conclude that IONPs induce complement-mediated cytokine secretion in human whole blood.
Author and source information

Authors: Wolf-Grosse S, Rokstad AM, Ali S, Lambris JD, Mollnes TE, Nilsen AM, Stenvik J.
Reference: MInt J Nanomedicine. 2017 May 23;12:3927-3940. doi: 10.2147/IJN.S136453. eCollection 2017.
Source: https://proxy.library.upenn.edu

 

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