Appl Environ Microbiol 2007, 73:4769–4775.PubMedCrossRef 45. Riley M, Abe T, Arnaud MB, Berlyn MK, Blattner FR, Chaudhuri RR, et al.: Escherichia coli K-12:a cooperatively developed annotation snapshot–2005. Nucleic Acids Res 2006, 34:1–9.PubMedCrossRef 46. Burland V, Shao Y, Perna NT, Plunkett G, Sofia HJ, Blattner FR: The complete DNA sequence and LY2109761 analysis of the large virulence plasmid of Escherichia coli O157:H7. Nucl Acids Res 1998, 26:4196–4204.PubMedCrossRef 47. Calderwood SB, Auclair F, Donohue-Rolfe A, Keusch GT, Mekalanos JJ: Nucleotide sequence of the Shiga-like toxin genes of Escherichia

coli LY3023414 solubility dmso . Proc Natl Acad Sci USA 1987, 84:4364–4368.PubMedCrossRef 48. Collett D: Modelling binary data. Boca Raton, Florida: Chapman & Hall/CRC; 1999. 49. Bühl A: SPSS Version 16: Einführung in die moderne Datenanalyse. BI2536 11th edition. Munich: Pearson Studium; 2008. Competing interests The authors declare that they have no competing interests. Authors’ contributions LB and PF played an integral role in the project conception and MB, PF and LB in method development. MB was mainly responsible for the design and execution of the experimental procedures. Data processing and statistical analysis was done by AM. Data analysis and interpretation of the results

was completed by all authors. LB was mostly responsible for the preparation of the manuscript. All authors have read and approved the final manuscript.”
“Background MYO10 In many environments bacteria exist as a complex, multi-species surface-associated community termed biofilm. Bacteria within these communities secrete an extracellular polymer matrix, form complex structures, and are

phenotypically distinct from their planktonic counterparts [1, 2], and are orders of magnitude more resistant to antibiotics and biocides than planktonic bacteria [3]. Furthermore, bacterial genes involved in biofilm formation are controlled by regulatory systems that also control the expression of virulence factors [4, 5]. Bacterial biofilms are a major barrier to healing in chronic wounds. In patients with underlying disease (i.e. diabetes, pulmonary disease), wounded epithelium offers an ideal environment for bacteria to form a biofilm due to susceptibility to contamination, availability of nutrients, and abundant surface area for attachment. Chronic-wound biofilms are not cleared by the host’s immune system and are resistant to traditional treatment strategies such as antibiotics [6]. Cutaneous wounds progress through three highly regulated phases of wound repair: inflammation, epithelialization, and tissue remodeling. Chronic wounds display abnormal progression through these phases including prolonged inflammation and failure to re-epithelialize. Currently, removal of the biofilm by frequent debridement is one of the most clinically effective treatments applied to chronic wounds [7].