Gold nanoparticles (AuNPs) are a promising platform for
biomedical
applications including therapeutics, imaging, and drug delivery. While
much of the literature surrounding the introduction of AuNPs into
cellular systems focuses on uptake and cytotoxicity, less is understood
about how AuNPs can indirectly affect cells via interactions with
the extracellular environment. Previous work has shown that the monocytic
cell line THP-1’s ability to undergo chemotaxis in response
to a gradient of monocyte chemoattractant protein 1 (MCP-1) was compromised
by extracellular polysulfonated AuNPs, presumably by binding to MCP-1
with some preference over other proteins in the media. The hypothesis
to be explored in this work is that the degree of sulfonation of the
surface would therefore be correlated with the ability of AuNPs to
interrupt chemotaxis. Highly sulfonated poly(styrenesulfonate)-coated
AuNPs caused strong inhibition of THP-1 chemotaxis; by reducing the
degree of sulfonation on the AuNP surface with copolymers [poly(styrenesulfonate-co-maleate) of different compositions], it was found that
medium and low sulfonation levels caused weak to no inhibition, respectively.
Small, rigid molecular sulfonate surfaces were relatively ineffective
at chemotaxis inhibition. Unusually, free poly(styrenesulfonate) caused
a dose-dependent reversal of THP-1 cell migration: at low concentrations,
free poly(styrenesulfonate) significantly inhibited MCP-1-induced
chemotaxis. However, at high concentrations, free poly(styrenesulfonate)
acted as a chemorepellent, causing a reversal in the cell migration
direction.