Abstract

Implant-associated infections are an increasingly severe burden on healthcare systems worldwide and many research activities currently focus on inhibiting microbial colonization of biomedically relevant surfaces. To obtain molecular-level understanding of the involved processes and interactions, we investigate the adsorption of synthetic adhesin-like peptide sequences derived from the type IV pili of the Pseudomonas aeruginosa strains PAK and PAO at abiotic model surfaces, i.e., Au, SiO2, and oxidized Ti. These peptides correspond to the sequences of the receptor-binding domain 128–144 of the major pilin protein, which is known to facilitate P. aeruginosa adhesion at biotic and abiotic surfaces. Using quartz crystal microbalance with dissipation monitoring (QCM-D), we find that peptide adsorption is material- as well as strain-dependent. At the Au surface, PAO(128–144) shows drastically stronger adsorption than PAK(128–144), whereas adsorption of both peptides is markedly reduced at the oxide surfaces with less drastic differences between the two sequences. These observations suggest that peptide adsorption is influenced by not only the peptide sequence, but also peptide conformation. Our results furthermore highlight the importance of molecular-level investigations to understand and ultimately control microbial colonization of surfaces.

Highlights

  • The past century has seen a continuous increase in the number of surgical procedures aimed at the restoration of body functions via the implantation of artificial biomaterials

  • To obtain molecular-level understanding of the involved processes and interactions, we investigate the adsorption of synthetic adhesin-like peptide sequences derived from the type IV pili of the Pseudomonas aeruginosa strains PAK and PAO at abiotic model surfaces, i.e., Au, SiO2, and oxidized Ti

  • Using quartz crystal microbalance with dissipation monitoring (QCM-D), we find that peptide adsorption is material- as well as strain-dependent

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Summary

Introduction

The past century has seen a continuous increase in the number of surgical procedures aimed at the restoration of body functions via the implantation of artificial biomaterials. While tremendous advances in the fields of reconstructive medicine and biomaterials science and engineering have resulted in highly efficient implants with low probability of rejection by the body, implant-associated infections have developed into a serious problem over the last two decades [1]. Suppressing implant-associated infections via the rational engineering of implant surfaces to render them resistant to microbial colonization has become a very important goal in the field of biomedical materials research [7]. For such engineering strategies to succeed, a detailed understanding of the molecular mechanisms that govern microbial colonization of abiotic surfaces is required

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