Extracellular polymeric substance (EPS)-degrading enzymes reduce staphylococcal surface attachment and biocide resistance on pig skin in vivo.

Autor: Kaplan JB; Department of Biology, American University, Washington, District of Columbia, United States of America., Mlynek KD; Department of Biology, American University, Washington, District of Columbia, United States of America., Hettiarachchi H; Department of Biology, American University, Washington, District of Columbia, United States of America., Alamneh YA; Wound Infections Department, Walter Reed Army Institute of Research, Silver Spring, Maryland, United States of America., Biggemann L; Wound Infections Department, Walter Reed Army Institute of Research, Silver Spring, Maryland, United States of America., Zurawski DV; Wound Infections Department, Walter Reed Army Institute of Research, Silver Spring, Maryland, United States of America., Black CC; Wound Infections Department, Walter Reed Army Institute of Research, Silver Spring, Maryland, United States of America., Bane CE; Wound Infections Department, Walter Reed Army Institute of Research, Silver Spring, Maryland, United States of America., Kim RK; Wound Infections Department, Walter Reed Army Institute of Research, Silver Spring, Maryland, United States of America., Granick MS; Department of Surgery, Rutgers New Jersey Medical School, Newark, New Jersey, United States of America.
Jazyk: angličtina
Zdroj: PloS one [PLoS One] 2018 Oct 10; Vol. 13 (10), pp. e0205526. Date of Electronic Publication: 2018 Oct 10 (Print Publication: 2018).
DOI: 10.1371/journal.pone.0205526
Abstrakt: Staphylococcal extracellular polymeric substances (EPS) such as extracellular DNA (eDNA) and poly-N-acetylglucosamine surface polysaccharide (PNAG) mediate numerous virulence traits including host colonization and antimicrobial resistance. Previous studies showed that EPS-degrading enzymes increase staphylococcal biocide susceptibility in vitro and in vivo, and decrease virulence in animal models. In the present study we tested the effect of EPS-degrading enzymes on staphylococcal skin colonization and povidone iodine susceptibility using a novel in vivo pig model that enabled us to colonize and treat 96 isolated areas of skin on a single animal in vivo. To quantitate skin colonization, punch biopsies of colonized areas were homogenized, diluted, and plated on agar for colony forming unit enumeration. Skin was colonized with either Staphylococcus epidermidis or Staphylococcus aureus. Two EPS-degrading enzymes, DNase I and the PNAG-degrading enzyme dispersin B, were employed. Enzymes were tested for their ability to inhibit skin colonization and detach preattached bacteria. The effect of enzymes on the susceptibility of preattached S. aureus to killing by povidone iodine was also measured. We found that dispersin B significantly inhibited skin colonization by S. epidermidis and detached preattached S. epidermidis cells from skin. A cocktail of dispersin B and DNase I detached preattached S. aureus cells from skin and increased their susceptibility to killing by povidone iodine. These findings suggest that staphylococcal EPS components such as eDNA and PNAG contribute to skin colonization and biocide resistance in vivo. EPS-degrading enzymes may be a useful adjunct to conventional skin antisepsis procedures in order to further reduce skin bioburden.
Competing Interests: We have read the journal's policy and the authors of this manuscript have the following competing interests: J.B.K. serves as an advisor for, owns equity in, and receives royalties from Kane Biotech, Inc., Winnipeg, Canada. This company is developing antibiofilm applications related to dispersin B. J.B.K. received research funding from Genentech, Inc., South San Francisco, CA, USA. This company may develop antibiofilm applications related to recombinant human DNase I. The authors K.D.M., H.H., Y.A.A., L.B., D.V.Z., C.C.B., C.E.B., R.K.K. and M.S.G. have no conflicts of interest or financial ties to disclose. These competing interests do not alter our adherence to PLOS ONE policies on sharing data and materials.
Databáze: MEDLINE
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