[1] Bigger JW. Treatment of staphylococcal infections with penicillin by intermittent sterilisation[J]. Lancet, 1944, 244:497–500[2] Spoering AL, Lewis K. Biofilms and planktonic cells of Pseudomonas aeruginosa have similar resistance to killing by antimicrobials[J]. J Bacteriol, 2001, 183(23): 6746-6751.[3] Keren I, Kaldalu N, Spoering A, et al. Persister cells and tolerance to antimicrobials[J]. FEMS Microbiol Lett, 2004, 230(1): 13-18.[4] Keren I, Shah D, Spoering A, et al. Specialized persister cells and the mechanism of multidrug tolerance in Escherichia coli[J]. J Bacteriol, 2004, 186(24): 8172-8180.[5] Lewis K. Persister cells, dormancy and infectious disease[J]. Nat Rev Microbiol, 2007, 5(1): 48-56.[6] Lewis K. Persister cells[J]. Annu Rev Microbiol, 2010, 64: 357-372.[7] LaFleur MD, Kumamoto CA, Lewis K. Candida albicans biofilms produce antifungal-tolerant persister cells[J]. Antimicrob Agents Chemother, 2006, 50(11): 3839-3846.[8] Ramage G, Wickes BL, Lopez-Ribot JL. Biofilms of Candida albicans and their associated resistance to antifungal agents[J]. Am Clin Lab, 2001, 20(7): 42-44.[9] Lafleur MD, Qi Q, Lewis K. Patients with long-term oral carriage harbor high-persister mutants of Candida albicans[J]. Antimicrob Agents Chemother, 2010, 54(1): 39-44.[10] Mulcahy LR, Burns JL, Lory S, et al. Emergence of Pseudomonas aeruginosa strains producing high levels of persister cells in patients with cystic fibrosis[J]. J Bacteriol, 2010, 192(23): 6191-6199.[11] 贾奋,亓庆国.用线虫模型研究白念珠菌生物膜中滞留菌对抗真菌治疗效果的影响[J]. 中华微生物学和免疫学杂志,2011年,第31卷(第10期): 588-591页 [12] Balaban NQ, Merrin J, Chait R, et al. Bacterial persistence as a phenotypic switch[J]. Science, 2004, 305(5690): 1622-1625.[13] Shah D, Zhang Z, Khodursky A, et al. Persisters: a distinct physiological state of E. coli[J]. BMC Microbiol, 2006, 6: 53.[14] Allison KR, Brynildsen MP, Collins JJ. Heterogeneous bacterial persisters and engineering approaches to eliminate them[J]. Curr Opin Microbiol, 2011, 14(5): 593-598.[15] Nystrom T. Stationary-phase physiology[J]. Annu Rev Microbiol, 2004, 58: 161-181.[16] Luidalepp H, Joers A, Kaldalu N, et al. Age of inoculum strongly influences persister frequency and can mask effects of mutations implicated in altered persistence[J]. J Bacteriol, 2011, 193(14): 3598-3605.[17] Walker GC. Understanding the complexity of an organism's responses to DNA damage[J]. Cold Spring Harb Symp Quant Biol, 2000, 65: 1-10.[18] Dorr T, Lewis K, Vulic M. SOS response induces persistence to fluoroquinolones in Escherichia coli[J]. PLoS Genet, 2009, 5(12): e1000760.[19] Dorr T, Vulic M, Lewis K. Ciprofloxacin causes persister formation by inducing the TisB toxin in Escherichia coli[J]. PLoS Biol, 2010, 8(2): e1000317.[20] Balaban NQ, Gerdes K, Lewis K, et al. A problem of persistence: still more questions than answers?[J]. Nat Rev Microbiol, 2013, 11(8): 587-591.[21] Johnson PJ, Levin BR. Pharmacodynamics, population dynamics, and the evolution of persistence in Staphylococcus aureus[J]. PLoS Genet, 2013, 9(1): e1003123.[22] Kim Y, Wood TK. Toxins Hha and CspD and small RNA regulator Hfq are involved in persister cell formation through MqsR in Escherichia coli[J]. Biochem Biophys Res Commun, 2010, 391(1): 209-213.[23] Wood TK, Knabel SJ, Kwan BW. Bacterial persister cell formation and dormancy[J]. Appl Environ Microbiol, 2013, 79(23): 7116-7121.[24] Hazan R, Sat B, Engelberg-Kulka H. Escherichia coli mazEF-mediated cell death is triggered by various stressful conditions[J]. J Bacteriol, 2004, 186(11): 3663-3669.[25] Schuster CF, Bertram R. Toxin-antitoxin systems are ubiquitous and versatile modulators of prokaryotic cell fate[J]. FEMS Microbiol Lett, 2013, 340(2): 73-85.[26] Hong SH, Wang X, O'Connor HF, et al. Bacterial persistence increases as environmental fitness decreases[J]. Microb Biotechnol, 2012, 5(4): 509-522.[27] Wang X, Wood TK. Toxin-antitoxin systems influence biofilm and persister cell formation and the general stress response[J]. Appl Environ Microbiol, 2011, 77(16): 5577-5583.[28] Leung V, Levesque CM. A stress-inducible quorum-sensing peptide mediates the formation of persister cells with noninherited multidrug tolerance[J]. J Bacteriol, 2012, 194(9): 2265-2274.[29] Patra P, Klumpp S. Population dynamics of bacterial persistence[J]. PLoS One, 2013, 8(5): e62814.[30] Hauryliuk V, Atkinson GC, Murakami KS, et al. Recent functional insights into the role of (p)ppGpp in bacterial physiology[J]. Nat Rev Microbiol, 2015, 13(5): 298-309.[31] Amato SM, Orman MA, Brynildsen MP. Metabolic control of persister formation in Escherichia coli[J]. Mol Cell, 2013, 50(4): 475-487.[32] Gerdes K, Maisonneuve E. Bacterial persistence and toxin-antitoxin loci[J]. Annu Rev Microbiol, 2012, 66: 103-123.[33] Nguyen D, Joshi-Datar A, Lepine F, et al. Active starvation responses mediate antibiotic tolerance in biofilms and nutrient-limited bacteria[J]. Science, 2011, 334(6058): 982-986.[34] Bernal P, Molina-Santiago C, Daddaoua A, et al. Antibiotic adjuvants: identification and clinical use[J]. Microb Biotechnol, 2013, 6(5): 445-449.[35] Drawz SM, Bonomo RA. Three decades of beta-lactamase inhibitors[J]. Clin Microbiol Rev, 2010, 23(1): 160-201.[36] Bernal P, Llamas MA. Promising biotechnological applications of antibiofilm exopolysaccharides[J]. Microb Biotechnol, 2012, 5(6): 670-673.[37] Flemming HC, Wingender J. The biofilm matrix[J]. Nat Rev Microbiol, 2010, 8(9): 623-633.[38] Rendueles O, Kaplan JB, Ghigo JM. Antibiofilm polysaccharides[J]. Environ Microbiol, 2013, 15(2): 334-346.[39] Valle J, Da Re S, Henry N, et al. Broad-spectrum biofilm inhibition by a secreted bacterial polysaccharide[J]. Proc Natl Acad Sci U S A, 2006, 103(33): 12558-12563.[40] Ma L, Jackson KD, Landry RM, et al. Analysis of Pseudomonas aeruginosa conditional psl variants reveals roles for the psl polysaccharide in adhesion and maintaining biofilm structure postattachment[J]. J Bacteriol, 2006, 188(23): 8213-8221.[41] Rendueles O, Travier L, Latour-Lambert P, et al. Screening of Escherichia coli species biodiversity reveals new biofilm-associated antiadhesion polysaccharides[J]. MBio, 2011, 2(3): e00043-00011.[42] Asif M, Acharya M. Quorum sensing: A nobel target for antibacterial agents[J]. Avicenna J Med, 2012, 2(4): 97-99.[43] Deep A, Chaudhary U, Gupta V. Quorum sensing and Bacterial Pathogenicity: From Molecules to Disease[J]. J Lab Physicians, 2011, 3(1): 4-11.[44] Pan J, Bahar AA, Syed H, et al. Reverting antibiotic tolerance of Pseudomonas aeruginosa PAO1 persister cells by (Z)-4-bromo-5-(bromomethylene)-3-methylfuran-2(5H)-one[J]. PLoS One, 2012, 7(9): e45778.[45] Pan J, Song F, Ren D. Controlling persister cells of Pseudomonas aeruginosa PDO300 by (Z)-4-bromo-5-(bromomethylene)-3-methylfuran-2(5H)-one[J]. Bioorg Med Chem Lett, 2013, 23(16): 4648-4651.[46] Pan J, Xie X, Tian W, et al. (Z)-4-bromo-5-(bromomethylene)-3-methylfuran-2(5H)-one sensitizes Escherichia coli persister cells to antibiotics[J]. Appl Microbiol Biotechnol, 2013, 97(20): 9145-9154.[47] Drissi F, Buffet S, Raoult D, et al. Common occurrence of antibacterial agents in human intestinal microbiota[J]. Front Microbiol, 2015, 6: 441.[48] Chen X, Zhang M, Zhou C, et al. Control of bacterial persister cells by Trp/Arg-containing antimicrobial peptides[J]. Appl Environ Microbiol, 2011, 77(14): 4878-4885.[49] Niepa TH, Gilbert JL, Ren D. Controlling Pseudomonas aeruginosa persister cells by weak electrochemical currents and synergistic effects with tobramycin[J]. Biomaterials, 2012, 33(30): 7356-7365. |