Our interest is in ultrathin coatings that can be applied to biomedical devices to mitigate device-related bacterial infections. The ability to produce a truly antimicrobial surface has only become feasible with the availability of antibacterials that compromise the integrity of the bacterial cell wall and cause death of the bacteria. Our aim is to produce coatings that will stop bacterial colonisation of the device surface, while allowing human cell attachment and spreading. Antimicrobial peptides are an abundant and diverse group of molecules that are found in many tissues and different cells and in a large variety of plant and animal species, and have been found to reduce infection and inflammation. These cationic peptides produce membrane disrupting behaviour in the bacteria, causing leakage and death. This work has explored the covalent surface grafting of the antimicrobial peptides LL37 (134-170), Magainin 2, and Parasin 1. We also explored the use of synthetic peptidomimetic analogues, which were kindly provided by Dr Runhui Liu from the Gellman group at the University of Wisconsin, USA.
The antimicrobial molecules are covalently anchored via amine groups on lysine residues or amine side chains on the synthetic polymers, reacting with aldehyde groups on materials surfaces.  A key question is whether the antimicrobial peptides and their synthetic analogues would still display antibacterial activity after covalent surface immobilisation, since activity might be compromised by either steric hindrance, or loss of protonable amine groups interacting with bacterial membranes, or a need to enter bacterial cytoplasm. We have found that LL37, Magainin 2 and Gellman’s synthetic peptidomimetic analogues showed excellent antimicrobial activity when grafted onto our surfaces. As previously reported by Gellman, they also showed excellent cell attachment and growth, which we have extended to primary cells. We have also shown using our wound assay, that one synthetic peptidomimetic polymer encourages cells to grow over the wound gap more rapidly and deters bacterial colonization of the wound area.