Effect of negative pressure on growth, secretion and biofilm formation of Staphylococcus aureus
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Negative pressure wound therapy (NPWT) has gained popularity in the management of contaminated wounds as an effective physical therapy, although its influence on the bacteria in the wounds remains unclear. In this study, we attempted to explore the effect of negative pressure conditions on Staphylococcus aureus, the most frequently isolated pathogen during wound infection. S. aureus was cultured in Luria–Bertani medium at subatmospheric pressure of −125 mmHg for 24 h, with the bacteria grown at ambient pressure as the control. The application of negative pressure was found to slow down the growth rate and inhibit biofilm development of S. aureus, which was confirmed by static biofilm assays. Furthermore, decreases in the total amount of virulence factors and biofilm components were observed, including α-hemolysin, extracellular adherence protein, polysaccharide intercellular adhesin and extracellular DNA. With quantitative RT-PCR analysis, we also revealed a significant inhibition in the transcription of virulence and regulatory genes related to wound infections and bacterial biofilms. Together, these findings indicated that negative pressure could inhibit the growth, virulence and biofilm formation of S. aureus. A topical subatmospheric pressure condition, such as NPWT, may be a potential antivirulence and antibiofilm strategy in the field of wound care.
KeywordsNegative pressure Staphylococcus aureus Virulence Biofilm formation
This research was supported by the National Natural Science Foundation of China (No. 81472112). The authors declare that they have no conflicts of interest.
- Assadian O, Assadian A, Stadler M, Diab-Elschahawi M, Kramer A (2010) Bacterial growth kinetic without the influence of the immune system using vacuum-assisted closure dressing with and without negative pressure in an in vitro wound model. Int Wound J 7:283–289. doi: 10.1111/j.1742-481X.2010.00686.x CrossRefPubMedGoogle Scholar
- Castro SL, Nelman-Gonzalez M, Nickerson CA, Ott CM (2011) Induction of attachment-independent biofilm formation and repression of Hfq expression by low-fluid-shear culture of Staphylococcus aureus. Appl Environ Microbiol 77:6368–6378. doi: 10.1128/aem.00175-11 PubMedCentralCrossRefPubMedGoogle Scholar
- Kairinos N, Solomons M, Hudson DA (2009) Negative-pressure wound therapy I: the paradox of negative-pressure wound therapy. Plast Reconstr Surg 123:589–598; discussion 599–600. doi: 10.1097/PRS.0b013e3181956551
- Moet GJ, Jones RN, Biedenbach DJ, Stilwell MG, Fritsche TR (2007) Contemporary causes of skin and soft tissue infections in North America, Latin America, and Europe: report from the SENTRY antimicrobial surveillance program (1998–2004). Diagn Microbiol Infect Dis 57:7–13. doi: 10.1016/j.diagmicrobio.2006.05.009 CrossRefPubMedGoogle Scholar
- Sadovskaya I, Chaignon P, Kogan G, Chokr A, Vinogradov E, Jabbouri S (2006) Carbohydrate-containing components of biofilms produced in vitro by some staphylococcal strains related to orthopaedic prosthesis infections. FEMS Immunol Med Microbiol 47:75–82. doi: 10.1111/j.1574-695X.2006.00068.x CrossRefPubMedGoogle Scholar
- Saxena V, Hwang CW, Huang S, Eichbaum Q, Ingber D, Orgill DP (2004) Vacuum-assisted closure: microdeformations of wounds and cell proliferation. Plast Reconstr Surg 114:1086–1096; discussion 1097–1088Google Scholar
- Steingrimsson S, Gottfredsson M, Gudmundsdottir I, Sjogren J, Gudbjartsson T (2012) Negative-pressure wound therapy for deep sternal wound infections reduces the rate of surgical interventions for early re-infections. Interact CardioVasc Thorac Surg 15:406–410. doi: 10.1093/icvts/ivs254 PubMedCentralCrossRefPubMedGoogle Scholar
- Ulrich M et al (2007) The staphylococcal respiratory response regulator SrrAB induces ica gene transcription and polysaccharide intercellular adhesin expression, protecting Staphylococcus aureus from neutrophil killing under anaerobic growth conditions. Mol Microbiol 65:1276–1287. doi: 10.1111/j.1365-2958.2007.05863.x CrossRefPubMedGoogle Scholar