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Fig. 7 | Particle and Fibre Toxicology

Fig. 7

From: Size and surface modification of silica nanoparticles affect the severity of lung toxicity by modulating endosomal ROS generation in macrophages

Fig. 7

Proposed model for regulation of chemokine expression in macrophages against silica particles with different properties. (Center) Nano-sized pristine silica NPs taken up by macrophages in the lungs were internalized in the endosomes. Interaction between silanol moieties and endosomal membrane does not cause endosomal rupture which can be visualized by Gal3 puncta, but may cause small damage to the membrane, which may lead to calcium and/or proton ion leakage into the cytosol, resulting in assemble of active NOX2 complexes and generation of endosomal ROS signals. Alternatively, certain receptors on the endosomal membrane might specifically recognize pristine silica NPs and activate signaling cascade, resulting in NOX2 activation. Endosomal ROS generated by activated NOX2 is supposed to diffuse into cytoplasm and end up inducing expression in proinflammatory chemokines through redox sensitive inflammatory pathways such as NF-kB. (Left) Efficacy in uptake of larger silica particles (3 μm) by macrophages is significantly reduced compared with nanoparticles, which results in attenuated inflammation. (Right) Nano-sized silica NPs with amine surface modification are internalized in the endosome of macrophages with an efficiency comparable to that of pristine NPs. However, attenuated endosomal ROS signals and inflammatory response were observed This may be because reduced silanol moieties on the surface of NPs may reduce the damage to endosomal membranes or impaired recognition of NH2-coated silica surfaces by the receptors

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