Self-Assembled Poly(ethylene glycol)-<i>co</i>-Acrylic Acid Microgels to Inhibit Bacterial Colonization of Synthetic Surfaces

We explored the use of self-assembled microgels to inhibit the bacterial colonization of synthetic surfaces both by modulating surface cell adhesiveness at length scales comparable to bacterial dimensions (∼1 μm) and by locally storing/releasing an antimicrobial. Poly­(ethylene glycol) [PEG] and poly­(ethylene glycol)-<i>co</i>-acrylic acid [PEG-AA] microgels were synthesized by suspension photopolymerization. Consistent with macroscopic gels, a pH dependence of both zeta potential and hydrodynamic diameter was observed in AA-containing microgels but not in pure PEG microgels. The microgels were electrostatically deposited onto poly­(l-lysine) (PLL) primed silicon to form submonolayer surface coatings. The microgel surface density could be controlled via the deposition time and the microgel concentration in the parent suspension. In addition to their intrinsic antifouling properties, after deposition, the microgels could be loaded with a cationic antimicrobial peptide (L5) because of favorable electrostatic interactions. Loading was significantly higher in PEG-AA microgels than in pure PEG microgels. The modification of PLL-primed Si by unloaded PEG-AA microgels reduced the short-term (6 h) <i>S. epidermidis</i> surface colonization by a factor of 2, and the degree of inhibition increased when the average spacing between microgels was reduced. Postdeposition L5 peptide loading into microgels further reduced bacterial colonization to the extent that, after 10 h of <i>S. epidermidis</i> culture in tryptic soy broth, the colonization of L5-loaded PEG-AA microgel-modified Si was comparable to the very small level of colonization observed on macroscopic PEG gel controls. The fact that these microgels can be deposited by a nonline-of-sight self-assembly process and hinder bacterial colonization opens the possibility of modifying the surfaces of topographically complex biomedical devices and reduces the rate of biomaterial-associated infection.