Abstract
PurposeMeticillin-resistant Staphylococcus aureus (MRSA) biofilm formation in humans is of serious clinical concern. Previous in vitro studies have been performed with biofilms grown only on inorganic substrates; therefore, we investigated the vancomycin (VCM) resistance of MRSA biofilms grown on skin tissue.MethodologyWe established a novel tissue substrate model, namely MRSA grown on segments of mouse skin tissue (dermal chips, DCs), and compared its resistance capacity against VCM with that of MRSA biofilms grown on plastic chips (PCs).Results/Key findingsFor one MRSA isolate, we found that the VCM MIC was identical (1.56 µg ml−1) for planktonic cultures and for biofilms-formed on PCs (PC-BF), although the minimum bactericidal concentration (MBC) increased to 6.25 µg ml−1 in PC-BF. On the contrary, the MIC and MBC for biofilms formed on DCs (DC-BF) significantly increased (25 and 50 µg ml−1, respectively). Furthermore, the minimum biofilm-eradicating concentration was higher for DC-BF (100 µg ml−1) than for PC-BF (25 µg ml−1). Using six MRSA strains, we found that in PC-BF, the c.f.u. number decreased with increasing VCM concentration, whereas in DC-BF, it greatly increased until the MIC was reached, accompanied by the formation of large colonies, thicker bacterial walls and the presence of many mitotic cells.ConclusionOur results indicate that the VCM resistance of MRSA was greater in DC-BF. We conclude that DCs may provide a specific environment for MRSA that enhances bacterial growth under cytotoxic VCM concentrations, and might be useful for the study of skin wound infections and the effects of antimicrobial drugs.
Highlights
Staphylococcus aureus is a Gram-positive, human commensal bacterium, commonly found on the skin of healthy people
Using six Meticillin-resistant S. aureus (MRSA) strains, we found that in plastic chips (PCs)-BF, the c.f.u. number decreased with increasing VCM concentration, whereas in dermal chips (DCs)-BF, it greatly increased until the MIC was reached, accompanied by the formation of large colonies, thicker bacterial walls and the presence of many mitotic cells
Our results indicate that the VCM resistance of MRSA was greater in DC-BF
Summary
Staphylococcus aureus is a Gram-positive, human commensal bacterium, commonly found on the skin of healthy people. Over the last half century, these bacteria have developed resistance to antimicrobial agents commonly prescribed in hospitals. Meticillin-resistant S. aureus (MRSA) is phenotypically associated with the presence of the penicillin-binding protein 2a (PBP2a) [1]. PBP2a has a significantly lower affinity for b-lactam antibiotics, which permits cell wall synthesis during antibiotic treatment, whereas wild-type penicillin-binding proteins are inactivated when bound to b-lactams. The bactericidal action of vancomycin (VCM) results predominantly from inhibition of cell wall biosynthesis [2]. VCM preferentially prevents the integration ofN-acetylmuramic acid (MurNAc)- and N-acetylglucosamine (GlcNAc)peptide subunits into the peptidoglycan matrix, which is the main structural component of the cell wall of Grampositive bacteria, including MRSA. The hydrophilic moiety of VCM is able to form hydrogen bonds with the terminal D-alanyl-D-alanine moieties of the MurNAc-/GlcNAcpeptides, preventing their incorporation into the peptidoglycan matrix. New antimicrobial agents have 000461 ã 2017 The Authors
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
