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The Antimicrobial Peptide TAT-Rasgap317-326 Inhibits the Formation and the Expansion

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The Antimicrobial Peptide TAT-Rasgap317-326 Inhibits the Formation and the Expansion bioRxiv preprint doi: https://doi.org/10.1101/2020.09.29.318378; this version posted September 29, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY-NC 4.0 International license. 1 The antimicrobial peptide TAT-RasGAP317-326 inhibits the formation and the expansion 2 of bacterial biofilms in vitro 3 Tytti Heinonen1, Simone Hargraves1, Maria Georgieva2, Christian Widmann2, Nicolas 4 Jacquier1.* 5 1Department of Laboratories, Institute of Microbiology, Lausanne University Hospital and 6 University of Lausanne, Lausanne, Switzerland 7 2Department of Physiology, University of Lausanne, Lausanne, Switzerland 8 9 Short title: Effect of TAT-RasGAP317-326 on biofilm formation and expansion 10 *Corresponding author: Nicolas Jacquier, Department of Laboratories, Institute of 11 Microbiology, Lausanne University Hospital and University of Lausanne, Rue du Bugnon 48, 12 CH-1011 Lausanne, Switzerland 13 Tel: +41 21 314 85 39 14 E-mail: [email protected] ; ORCID: 0000-0002-1974-8161 15 16 Number of figures: 3 17 Number of tables: 1 18 1 bioRxiv preprint doi: https://doi.org/10.1101/2020.09.29.318378; this version posted September 29, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY-NC 4.0 International license. 19 Abstract 20 Biofilms are structured aggregates of bacteria embedded in a self-produced matrix. Pathogenic 21 bacteria can form biofilms on surfaces and in tissues leading to nosocomial and chronic 22 infections. While antibiotics are largely inefficient in limiting biofilm formation and expansion, 23 antimicrobial peptides (AMPs) are emerging as alternative anti-biofilm treatments. In this study, 24 we explore the effect of the newly described AMP TAT-RasGAP317-326 on Acinetobacter 25 baumannii, Pseudomonas aeruginosa and Staphylococcus aureus biofilms. We observe that 26 TAT-RasGAP317-326 inhibits the formation of biofilms at concentrations equivalent or two times 27 superior to the minimal inhibitory concentration (MIC) of the corresponding planktonic bacteria. 28 Moreover, TAT-RasGAP317-326 limits the expansion of A. baumannii and P. aeruginosa 29 established biofilms at concentrations 2-4 times superior to the MIC. These results further 30 confirm the potential of AMPs against biofilms, expand the antimicrobial potential of TAT- 31 RasGAP317-326 and support further development of this peptide as an alternative antimicrobial 32 treatment. 33 34 Keywords: biofilms, antimicrobial peptide, antibiotic resistance, TAT-RasGAP317-326 35 2 bioRxiv preprint doi: https://doi.org/10.1101/2020.09.29.318378; this version posted September 29, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY-NC 4.0 International license. 36 Introduction 37 The emergence of antibiotic resistance is a major threat to public health. Infections 38 caused by multidrug resistant bacteria are an increasing concern, leading to disabilities and 39 possibly death [1]. One limitation in the development of novel antibiotics is the use of free-living 40 (also called planktonic) bacteria in axenic medium as model system. This model is not 41 representative of infections, as the majority of them are caused by multicellular aggregates of 42 bacteria in a self-produced matrix, called biofilms. [2]. The formation of biofilms is dynamic and 43 triggered by signals such as nutrient limitation, antibiotic exposure and oxygen availability [3]. 44 The matrix embedding the biofilm is composed of polysaccharides, DNA and proteins, and 45 forms a scaffold for bacterial attachment, protects bacteria from external insults, and enables 46 a compartmentalisation of the biofilms with distinct bacterial subpopulations [2, 4]. 47 Pathogenic bacteria, including Acinetobacter baumannii, Pseudomonas aeruginosa 48 and Staphylococcus aureus, can form biofilms on medical devices implanted in humans, 49 develop in some tissues, e.g. lungs, teeth and skin, and may persist on healthcare surface [5, 50 6]. Moreover, bacteria present in biofilms can be 10 to1000 times more resistant to antibiotics 51 than planktonic bacteria [7]. Bacteria contained in biofilms strongly differ from planktonic 52 bacteria regarding both their gene expression profile and their functional properties. Moreover, 53 bacterial subpopulations composing biofilms are heterogeneous, further complicating biofilm 54 treatment. Current biofilm treatment is tedious and resembles cancer therapy starting with the 55 surgical removal of the biofilm followed by administration of antimicrobials [8]. This strategy is 56 not optimal since antimicrobials are often unable to eradicate all bacterial subpopulations 57 embedded in the biofilm. Moreover, this treatment may not completely disrupt the biofilm 58 scaffold, potentially allowing its colonization by other microorganisms. The combination of 59 intrinsic antibiotic resistance with resistance properties provided by the biofilm organisation 60 renders these nosocomial infections highly challenging to treat. We thus need alternatives to 61 classical antibiotics to treat biofilms formed by resistant pathogens. 3 bioRxiv preprint doi: https://doi.org/10.1101/2020.09.29.318378; this version posted September 29, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY-NC 4.0 International license. 62 Antimicrobial peptides (AMPs) could be such an alternative. AMPs are short peptides 63 (up to 100 amino acids) produced by all living organisms as a defence mechanism that usually 64 target a broad range of pathogens [9]. While the ability of bacteria to develop resistance 65 towards AMPs is debated [10], pathogens carrying resistance genes to one or multiple 66 antibiotics often show increased sensitivity towards AMPs [11, 12]. Some AMPs, alone or 67 combined with antibiotics, act both on the inhibition of biofilm formation and on the disruption 68 of mature biofilm [13]. 69 TAT-RasGAP317-326 is a chimeric peptide consisting of the cell-permeable HIV peptide 70 TAT48-57 linked to a 10-amino acid sequence of the Src Homology 3 Domain (SH3 domain) of 71 p120 RasGAP [14]. TAT-RasGAP317-326 was first described for its anticancer properties, being 72 able to sensitise cancer cells to anticancer therapies [15-17], directly kill cancer cells [18] and 73 display anti-metastatic effect [19]. More recently, we showed that TAT-RasGAP317-326 exerts a 74 broad antimicrobial activity against both Gram-positive and Gram-negative human pathogens 75 including A. baumannii, P. aeruginosa and S. aureus [20]. Like other AMPs, TAT-RasGAP317- 76 326 is positively charged and contains several arginine and tryptophan residues. Arginine 77 residues may interact with the negatively charged bacterial membrane while tryptophan may 78 insert in the bacterial membrane [21, 22]. These interactions may enable AMPs to translocate 79 in the bacteria without disrupting membrane and to target intracellular components. While the 80 tryptophan at position 317 of RasGAP domain is essential for the antimicrobial activity of TAT- 81 RasGAP317-326, the mode of action of this peptide remains unknown. 82 In this report, we questioned the potential effect of TAT-RasGAP317-326 on biofilm 83 formation and on mature biofilm expansion. We show that TAT-RasGAP317-326 inhibits the 84 formation of A. baumannii, P. aeruginosa and S. aureus biofilms in vitro at concentrations equal 85 or 2 times the MIC of planktonic bacteria. Moreover, treatment of mature biofilms with TAT- 86 RasGAP317-326 reduces the expansion of A. baumannii and P. aeruginosa biofilms, but, similarly 87 to other tested antibiotics and AMPs, cannot completely eradicate the biofilm scaffold. These 4 bioRxiv preprint doi: https://doi.org/10.1101/2020.09.29.318378; this version posted September 29, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY-NC 4.0 International license. 88 results highlight the potential of TAT-RasGAP317-326 in the prevention and treatment of biofilms 89 and encourage further development of AMPs as alternative antimicrobial compounds. 90 5 bioRxiv preprint doi: https://doi.org/10.1101/2020.09.29.318378; this version posted September 29, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY-NC 4.0 International license. 91 Material and methods 92 Bacterial strains and growth conditions 93 Acinetobacter baumannii ATCC 19606 (A. baumannii) and Staphylococcus aureus 94 ATCC 29213 (S. aureus) were from American Type Culture Collection (ATCC; Manassas, VA). 95 Pseudomonas aeruginosa PA14 (P. aeruginosa) was obtained from Professor Leo Eberl 96 (Department of Plant and Microbial Biology, University of Zürich, Switzerland). Bacteria were 97 routinely grown in Mueller-Hinton broth (A. baumannii), tryptic soy broth (TSB; S. aureus) and 98 Luria-Bertani broth (LB; P. aeruginosa). 99 Peptides and antibiotics 100 TAT-RasGAP317-326 is a retro-inverso peptide (i.e. reversed direction compared to 101 natural sequence including D-amino acids) with an antimicrobial activity [20] composed of 102 amino acids 48-57 of HIV TAT protein (RRRQRRKKRG) and 317-326 of human RasGAP 103 protein (DTRLNTVWMW) linked with two glycines. TAT-RasGAP317-326 was synthesized by 104 SBS Genetech (Beijing, China). Ciprofloxacin, tetracycline and gentamicin were from 105 Applichem (Darmstadt, Germany), rifampicin and polymyxin B from Sigma-Aldrich (Saint- 106 Louis, MO), and melittin from Enzo Life Sciences (Farmingdale, NY).
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