Preventing the bacterial colonization of tissue-contacting biomedical devices is a key scientific challenge rich with potential clinical impact. Much research has concentrated on antimicrobial modification of device surfaces either by incorporating continuous elution mechanisms or by covalent surface tethering.  Both strategies have shortcomings.  As an alternative, we are studying a microgel-based approach that can flexibly modulate the bacteria-interactive surface properties.  Microgels provide a controllable combination of size, soft mechanical properties, and network behavior. Notably, polyelectrolyte microgels can be electrostatically deposited to form sub-monolayer microgel coatings on complex 3-D device surfaces. Much of the underlying surface remains exposed to interact with mammalian cells and promote healing while the microgels impart antimicrobial properties to inhibit infection. We have shown that the size and spatial distribution of antifouling PEG-based microgels critically controls the competing requirements for bacterial repulsion and tissue-cell adhesion and proliferation. Incorporating antimicrobials into the microgels brings a second line of defence against bacterial colonization. To this end, we have concentrated on colloidal poly(acid) microgels such as poly(acrylic acid) (PAA) synthesized by suspension polymerization or membrane emulsification. After deposition, their internal negative charge enables loading by cationic antimicrobials via a second self-assembly step driven by antimicrobial-microgel complexation. Analogous to a cation exchange column, the drugs remain complexed when exposed to salt-free buffer at pH 7.4 but can be released as the ionic strength is increased. Importantly, we have identified several antimicrobials, notably antimicrobial peptides with high positive charge and hydrophobicity, that remain sequestered under physiological pH and ionic strength for weeks or more.  These antimicrobials are nevertheless released when the loaded microgels are contacted by bacteria, a process that kills the bacteria. We speculate that this antimicrobial is driven by the high concentration of negative charge and hydrophobicity associated with the bacterial cell envelope. Tissue cells such as osteoblasts or macrophages are, however, unable to similarly trigger release. Such bacteria-triggered release represents a new mechanism with which to create a so-called self-defensive surface with which to prevent device infection.

Controlling bacteria-material interactions via polyelectrolyte microgels

Macromolecular Chemistry: The Second Century

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ACS Spring 2020 National Meeting & Expo

The official archive and repository for all ACS Meetings & Expositions abstracts and select posters or presentations.