ライフサイエンスコーパス: persister

1 cteriostatic and does not kill drug-tolerant persisters.

2 detection distinguished ADHD remitters from persisters.

3 Hydrolyzing corrupted tRNA resuscitates persisters.

4 al component TolC, show higher expression in persisters.

5 les in S. aureus did not affect the level of persisters.

6 illin-resistant Staphylococcus aureus (MRSA) persisters.

7 y a small population of dormant cells called persisters.

8 ultures, a finding that is characteristic of persisters.

9 e the activity of quinolones against E. coli persisters.

10 ght be due to the existence of drug-tolerant persisters.

11 ssociated proteins were unique for ofloxacin persisters.

12 ignificantly higher in resolvers compared to persisters.

13 ic inheritance causes increased frequency of persisters.

14 ess the most therapeutic potential to combat persisters.

15 rrupting a target in dormant cells will kill persisters.

16 que stress response signature: these are the persisters.

17 pically resistant cells, the latter known as persisters.

18 sence of biofilms and metabolically inactive persisters.

19 nts and young adults with childhood ADHD (87 persisters, 23 remitters) and 169 age-matched control pa

20 induces the formation of both VBNC cells and persisters, a finding not previously described for eithe

21 antibiotic tolerance is related to bacterial persisters, a sub-population of bacteria phenotypically

22 ormation of Mycobacterium tuberculosis (Mtb) persisters achieves a high level of antibiotic-tolerance

23 le has no effect on the formation of E. coli persisters against an aminocoumarin, novobiocin, which t

24 stimulates the formation of Escherichia coli persisters against quinolone antibiotics which target th

25 le to eradicate MRSA biofilms or non-biofilm persisters alongside 14.

26 rge these two fields of research: antibiotic persisters and host-pathogen interactions.

27 tment is not effective against infections by persisters and MDR-Mtb, novel therapeutics are needed.

28 ways, whereas ClpA was unique for ampicillin persisters and nucleoid-associated proteins were unique

29 y of network structures were compared across persisters and remitters using a permutation test.

30 nce-monitoring task distinguish between ADHD persisters and remitters.

31 s have an important role in the formation of persisters and several studies show that they can form i

32 n the basis for translational suppression in persisters and suggest how persisters survive exposure t

33 ngs show that fluoroquinolones damage DNA in persisters and that the ensuing SOS response accelerates

34 ADHD remitters differed from persisters and were indistinguishable from control parti

35 ericidal, killed drug-tolerant mycobacterial persisters, and rapidly cleared M. tuberculosis infectio

36 r formation of both ampicillin and ofloxacin persisters, and we demonstrated that higher synthesis of

37 Persisters are a sub-population of genetically sensitive

38 Bacterial persisters are able to tolerate high levels of antibioti

39 Rare persisters are already present in naive T-ALL population

40 ntified as contributing to the production of persisters are analogous to the so-called mutator genes;

41 Bacterial persisters are antibiotic-tolerant cells, but little is

42 Persisters are associated with chronic infections and an

43 Persisters are dormant phenotypic variants of bacterial

44 Persisters are in a dormant metabolic state, even while

45 Persisters are metabolically dormant, so they are highly

46 Persisters are multidrug-tolerant bacteria that could ac

47 Persisters are nongrowing, transiently antibiotic-tolera

48 are, phenotypically resistant subpopulation, persisters are notoriously hard to study and define.

49 Persisters are phenotypic variants of normal cells and p

50 Persisters are phenotypic variants of regular cells that

51 Persisters are phenotypic variants present within isogen

52 Bacterial persisters are phenotypic variants that form from the ac

53 Here, we show that S. aureus persisters are produced due to a stochastic entrance int

54 Bacterial persisters are rare phenotypic variants that temporarily

55 Bacterial persisters are rare, phenotypically distinct cells that

56 Using computerized tracking we show that persisters are small at birth and slowly replicating.

57 Bacterial persisters are thought to underlie the relapse of chroni

58 We find that persisters are unlikely to derive from bacteria with low

59 ic and pharmacogenomic screens revealed that persisters are vulnerable to inhibition of the transcrip

60 cells in many bacterial populations, called persisters, are much less sensitive to antibiotic treatm

61 more, this antibiotic eliminated challenging persisters as well as established biofilms.

62 rmant bacteria at pH 5.8, and nonreplicating persisters at low oxygen tension of </= 10 parts per bil

63 s (MRSA), including replicating, biofilm and persister bacterial cells, and also disperses biofilm bi

64 counts 3-4 weeks into therapy may identify a persister bacterial phenotype.

65 This subpopulation was distinct from persisters, became predominant in colistin, returned to

66 e, these findings raise the possibility that persisters behave as an evolutionary reservoir from whic

67 resistance mechanisms that can expand from a persister bottleneck is unknown.

68 Several approaches were proposed to kill persisters by altering their metabolism, obviating the n

69 omes a fairly nonspecific protease and kills persisters by degrading over 400 proteins, forcing cells

70 These persisters can be visualized using dual-reporter mycobac

71 Microbial persisters can cause recurrent or intractable infections

72 dent growth arrest, explaining how bacterial persisters can resume growth.

73 ls and provide new insight into a potential "persister cancer cell" phenotype.

74 stress, reduces colonization and attenuates persister cell and biofilm formation, suggesting that me

75 Loss of GPX4 function results in selective persister cell ferroptotic death in vitro and prevents t

76 orm studies on the role of the Psp system in persister cell formation and cell envelope protection in

77 This prevention of both persister cell formation and drug resistance leads ultim

78 in and repressing stress responses to reduce persister cell formation by 21-fold.

79 of ppGpp so that the underlying mechanism of persister cell formation could be explored.

80 PI-7 expressed genes related to dormancy and persister cell formation during the late decay phase, wh

81 T, indicating that multiple pathways lead to persister cell formation in C. crescentus.

82 characterized to participate in biofilm and persister cell formation in Escherichia coli.

83 Production of YafQ increased persister cell formation with multiple antibiotics, and

84 nonstringent processes, including virulence, persister cell formation, and biofilm production.

85 ese TAS, which are classically implicated in persister cell formation, are also induced during incuba

86 s have been postulated to be responsible for persister cell formation, we investigated the influence

87 the YafQ/DinJ Escherichia coli TA system on persister cell formation.

88 uch as phage inhibition, gene regulation and persister cell formation.

89 e TA system has only a minor contribution to persister cell formation.

90 t potent biofilm-eradicating agent (>/=99.9% persister cell killing) against MRSA (MBEC < 10 muM), MR

91 The persister cell pool constitutes a reservoir from which d

92 indings quantify pre-existing resistance and persister cell populations, which are essential for the

93 ds directly for stimulating Escherichia coli persister cell resuscitation, we identified that 2-{[2-(

94 nd are recognized by macrophages, while in a persister cell status, and upon awakening due to exposur

95 tants from GM-CSF treated P. aeruginosa PAO1 persister cell suspensions were found cidal to the pyoci

96 Consequently, we demonstrate that persister cells acquire a dependency on GPX4.

97 Relative to GSI-sensitive cells, persister cells activate distinct signaling and transcri

98 bitors effectively inhibits the emergence of persister cells and may represent a new therapeutic stra

99 Persister cells are a multi-drug tolerant subpopulation

100 In contrast, awakened S. aureus persister cells are able to initiate infections in A. th

101 Bacterial persister cells are highly tolerant to antibiotics and c

102 Our results show that S. aureus persister cells are not able to initiate infections in A

103 Tolerant and persister cells are thought to underlie biofilm-related

104 he role of FGFR in promoting the survival of persister cells been elucidated.

105 or HipA-mediated antibiotic persistence, but persister cells can form in the absence of all hipBA ope

106 Translation remodelling in persister cells coincides with an increased N6-methylade

107 istant cell state underlies the behaviour of persister cells derived from a wide range of cancers and

108 mmunities of enriched populations containing persister cells encased within a protective extracellula

109 ibit quiescence and reduce the population of persister cells formed by the uropathogenic strain, CFT0

110 between therapy failure and the presence of persister cells has started to emerge.

111 factors (in the absence of immune cells) on persister cells have not been studied.

112 ysical and molecular relatedness of VBNC and persister cells in a standardized model organism.

113 suggested to play a part in the formation of persister cells in mycobacteria.

114 M), as well as the effective killing of MRSA persister cells in non-biofilm cultures.

115 e investigated whether Staphylococcus aureus persister cells initiate an infection and are recognized

116 and found that the immune clearance rate of persister cells is a key feature.

117 The most differentially up-regulated gene in persister cells is mqsR, a gene that, with the antitoxin

118 timulating factor (GM-CSF) can sensitize the persister cells of Pseudomonas aeruginosa PAO1 and PDO30

119 nthesis via Ras can lead to formation of AmB-persister cells regardless of whether the cells are in p

120 cal strategy for preventing the emergence of persister cells remains elusive.

121 Bacterial persister cells represent a subpopulation of cells that

122 Hence, persister cells resuscitate via activation of RluD.

123 We found that persister cells still form, although at lower levels, in

124 Persister cells survive antibiotic and other environment

125 Dormant persister cells that are tolerant to killing by antibiot

126 Targeting persister cells therefore presents a therapeutic opportu

127 nti-cancer drug mitomycin C (MMC) eradicates persister cells through a growth-independent mechanism.

128 eract, leading to enhanced susceptibility of persister cells to antibiotics.

129 Furthermore, exposure of S. aureus persister cells to cis-DA led to a loss of tolerance to

130 that stimulates Mtb respiration and converts persister cells to metabolically active cells.

131 Cancer persister cells tolerate anticancer drugs and serve as t

132 y, including genomic stability, formation of persister cells under antibiotic stress, and resistance

133 acteremia was considered, the growth rate of persister cells was also found to be a key feature.

134 In addition, macrophage engulfment of persister cells was significantly lower than engulfment

135 Persistent bacteria, including persister cells within surface-attached biofilms and slo

136 Persister cells, a tolerant cell sub-population, are com

137 role of efflux pumps and the development of persister cells, are the topics of the final article by

138 s and induces growth arrest and apoptosis in persister cells, at doses well tolerated by GSI-sensitiv

139 gellar motility and pyocin production in the persister cells, but not the normal cells of P. aerugino

140 oad-spectrum compound capable of eliminating persister cells, meriting investigation as a new approac

141 iated with initially surviving drug-tolerant persister cells, which can seed bona fide genetic mechan

142 siology, and contribute to the occurrence of persister cells.

143 increased the number of active ribosomes in persister cells.

144 death and production of antibiotic-tolerant persister cells.

145 gy to rapidly purify ribosome complexes from persister cells.

146 ce for the clinical significance of VBNC and persister cells.

147 osomal RNA and protein components from these persister cells.

148 ively increased translation and is lethal to persister cells.

149 tibiotics against Burkholderia thailandensis persister cells.

150 T-ALL resistance, identifying GSI-tolerant 'persister' cells that expand in the absence of NOTCH1 si

151 underlying the survival of residual cancer 'persister' cells.

152 es error-prone polymerases in drug-tolerant (persister) cells.

153 All bacteria form persisters, cells that are multidrug tolerant and theref

154 sis (Mtb) cells, but the remaining cells are persisters, cells with decreased metabolic rate, refract

155 of this phenomenon, as well as to assess the persisters' clinical relevance.

156 ouble-hit lymphoma evolves from outgrowth of persister clones displaying loss of 18q21 amplicons that

157 ndant, making it challenging to develop anti-persister compounds.

158 er, populations derived from fluoroquinolone persisters contain significantly greater quantities of a

159 her with the invention of new tools to study persisters, could have important implications for the de

160 Here we compare persister-derived, erlotinib-resistant colonies that aro

161 th otherwise lethal drugs, the drug-tolerant persisters (DTPs), exhibit a repressed chromatin state c

162 rise to small populations of "drug tolerant persisters" (DTPs) (Figure 1B-C) that were reversed duri

163 ug-sensitive cells, so-called drug-tolerant "persisters" (DTPs), can survive cytotoxic drug exposure

164 single-cell analysis to identify Salmonella persisters during infection.

165 , so too does the need for clinically useful persister-eradication strategies.

166 l model of resistance development, including persister evolution and preexisting resistance, solely b

167 Assuming only persister evolution would require very high mutation ind

168 of only preexisting resistant cells or only persister evolution, it is not possible to explain the o

169 Interestingly, the lag time distribution of persisters exhibited a long tail captured by a power-law

170 with MDD are related to longitudinal course: persisters exhibited a more densely connected network at

171 eveloped, adopting the notion that bacterial persisters exist in the biofilms together with regulator

172 Our results show that (i) ribosomes in persisters exist largely as inactive ribosomal subunits,

173 Since Persister-FACSeq can be applied to study persistence to

174 As a proof-of-concept, we used Persister-FACSeq on a library of reporters to study gene

175 Here we developed Persister-FACSeq, which is a method that uses fluorescen

176 following ofloxacin treatment, we find that persisters filament extensively and induce impressive SO

177 Although persisters form during normal growth from native stresse

178 e we show that wild-type HipA contributes to persister formation and that high-persister hipA mutants

179 trant infections, the mechanisms that induce persister formation are not fully understood.

180 ort that Samonella toxin TacT contributes to persister formation by acetylating tRNA, a novel mechani

181 e exhibits qualitatively similar behavior to persister formation for short dosing times, and similar

182 Persister formation has been attributed to alterations i

183 is study, we find that salicylate can induce persister formation in Escherichia coli via generation o

184 The mechanism of persister formation in Gram-positive bacteria is unknown

185 and found that a persister killer, but not a persister formation inhibitor, could provide for an effe

186 pathways leading to growth mode-independent persister formation is important for developing novel st

187 del, we have reconstructed a molecular-level persister formation pathway from initial stress (glucose

188 entify the shared and unique elements of the persister formation pathways.

189 ynamics by considering adaptive response and persister formation separately.

190 that loss of clpA, ssrA, or smpB eliminated persister formation through relaxation of the stringent

191 toxin-antitoxin modules have been linked to persister formation(4-6).

192 t over-expressed HipA protein, which induces persister formation, and were treated with ampicillin to

193 n antibiotic's mode of action when analyzing persister formation, demonstrate that individual stresse

194 ong multiple biological pathways involved in persister formation, indicates that persisters implement

195 intimately linked to bacterial pathogenesis, persister formation, stress responses, and ribosome inte

196 d antibiotics together effectively attenuate persister formation, suggesting a combination strategy t

197 ial and metabolism, may play a broad role in persister formation.

198 thereby inhibiting translation and promoting persister formation.

199 titoxin modules contributed to intracellular persister formation.

200 iverse signalling roles, including a role in persister formation.

201 as a prime target for reducing the number of persisters formed in nutrient-depleted, non-growing popu

202 ters into metabolic quiescence (dormancy) as persister forms.

203 at show a characteristic correlation between persister frequency and the number of toxin-antitoxin sy

204 erexpression of these toxins often increases persister frequency in a defined population.

205 The emergence of persisters from dormancy after antibiotic withdrawal lea

206 Biofilms shield persisters from the immune system, suggesting that an an

207 Accordingly, persister GSCs upregulate, and are dependent on, the his

208 For a long time, persisters have been assumed to be nonreplicating dorman

209 While antibiotic persisters have been extensively studied over the last d

210 Persisters have been hypothesized to underlie the recalc

211 Persisters have traditionally been thought of as metabol

212 such knowledge has remained elusive because persisters have yet to be segregated from other cell typ

213 nstrate that individual stresses can produce persister heterogeneity, and emphasize the importance of

214 ributes to persister formation and that high-persister hipA mutants cause multidrug tolerance in urin

215 olved in persister formation, indicates that persisters implement a positive defense against antibiot

216 h rapamycin also increased the proportion of persisters in Candida albicans and Candida glabrata.

217 ary phase metabolism in generation of type I persisters in Escherichia coli, which are those that are

218 s stimulate the formation of fluoroquinolone persisters in Escherichia coli.

219 Due to the low frequencies of persisters in growing bacterial cultures and the complex

220 tence, report evidence for the importance of persisters in infection, and highlight studies that brid

221 t bactericide for a broad range of bacterial persisters, including commensal Escherichia coli K-12 as

222 We show that the stimulation of quinolone persisters is due to indole pulse, rather than persisten

223 monstrate that VBNC cells are present during persister isolation experiments, further indicating that

224 nt and relapsing bacteremia and found that a persister killer, but not a persister formation inhibito

225 respiration during stationary phase reduces persister levels by up to approximately 1,000-fold.

226 e, we adapted a biofilm culture to model Mtb persister-like bacilli (PLB) and demonstrated that PLB u

227 Persister-like cells and genomic amplifications of IRS2

228 In this Review, we discuss protozoan persister-like cells that have been linked to persistent

229 ory to drug treatment, which we refer to as 'persister-like cells'.

230 ggest that host immune factors and bacterial persisters may directly interact, leading to enhanced su

231 the underlying conclusion that adaptive and persister mechanism provide protection for different cha

232 or relA, implicated in the regulation of the persister metabolic state.

233 WR12 and D-IK8 were able to eradicate persisters, MRSA in stationary growth phase, and showed

234 understand the pathogen-host interactions of persister MRSAs in vivo.

235 We also determine that the high-persister mutant strain of Escherichia coli, HipQ, is as

236 Perplexingly, high-persister mutations map to the N-subdomain-1 of HipA far

237 Persisters (n = 253) had a higher baseline IDS sum score

238 had the largest difference in importance in persisters' network compared with that of remitters (Coh

239 amage, which has led to the supposition that persister offspring give rise to antibiotic-resistant mu

240 ne function have the potential to eradicate "persister" organisms and delay the emergence of resistan

241 icated that formation and maintenance of the persister phenotype are regulated by suppressing transla

242 lipid bodies has been proposed to identify a persister phenotype of Mycobacterium tuberculosis cells.

243 The ras1, ras2 and tor1 mutants had a high-persister phenotype similar to wild-type biofilm and pla

244 of barcoded lineages adopt a Notch-dependent persister phenotype that sustains them through early dru

245 nd next generation sequencing to interrogate persister physiology and its heterogeneity.

246 Knowledge of persister physiology would illuminate avenues for therap

247 n resulted in a significant depletion of the persister population in response to various classes of a

248 rvival was constrained to a slow-replicating persister population of S. Typhimurium induced within th

249 Isoniazid induced a drug-tolerant persister population only when necrotic lesions were pre

250 rvival, one possible hypothesis is that this persister population requires the glucose redirected to

251 tumor cell population versus a slow-growing persister population that is the precursor of acquired T

252 r findings indicate that upon awakening of a persister population the cells regain their ability to i

253 ulted in the most efficient reduction in the persister population.

254 wever, combining preexisting resistance with persister populations can explain the observed tumor vol

255 sis drugs that are active against dormant or persister populations of Mycobacterium tuberculosis.

256 who progressed on EGFR TKI as surrogates for persister populations, we performed whole-genome CRISPR

257 gradient on the recovery of B. thailandensis persister populations.

258 d the 11th module, hipBA, encodes HipA (high persister protein A) kinase, which inhibits glutamyl tRN

259 model reveals the crucial role played by the persisters, quorum sensing molecules, and growth factors

260 at diauxie-dependent formation of ampicillin persisters required RelA and that loss of clpA, ssrA, or

261 Here, modeling of BETi-persister/resistance (BETi-P/R) in human postmyeloprolif

262 Eventually, persisters resume growth, accounting for relapses of inf

263 Some persisters resumed intracellular growth after phagocytos

264 RNA RybB which represses rluD led to faster persister resuscitation.

265 In particular, a sub-group termed persisters show high tolerance to antibiotics.

266 sly produces metastable phenotypic variants (persisters), some of which represent stem-like states th

267 Thus, the drug-tolerant persister state does not limit--and may even provide a l

268 ular metabolite that has been linked to this persister state is guanosine tetraphosphate (ppGpp), the

269 h are often linked to cell growth, promote a persister state regardless of the underlying physiologic

270 trong selective drug pressure by entering a 'persister' state of negligible growth.

271 Further, persister status is generated via adaptive super-enhance

272 cal and simulation results probe the optimal persister strategy, revealing results that are consisten

273 Previous studies have found that persisters survive antibiotic treatment by maintaining a

274 al suppression in persisters and suggest how persisters survive exposure to multiple antibiotics.

275 a subpopulation of bacterial cells known as persisters survives by halting metabolism.

276 f cells is killed but a subpopulation called persisters survives the treatment.

277 pH induced nonstable SCVs and nonreplicating persisters that are capable of regrowth.

278 ment is thought to be due to the presence of persisters that are non-growing, antibiotic-insensitive

279 plication or the formation of nonreplicating persisters that could provide a reservoir for relapsing

280 ed subpopulation of reversibly drug-tolerant persisters that is dynamically maintained within a wide

281 of stresses in the host and form nongrowing persisters that survive both antibiotics and host immune

282 pulation of growing and nongrowing cells, or persisters, that exist under normal conditions, rather t

283 the Salmonella population forms non-growing persisters through the action of toxin-antitoxin modules

284 L-arginine and gentamicin against planktonic persisters through time-kill curves of late stationary-p

285 hesis of the alarmone was needed to increase persisters to ampicillin compared to ofloxacin.

286 Here, we examine how persisters to ampicillin form from the same metabolic st

287 osynthesis, as evidenced by the formation of persisters to antibiotics that target enzymes in differe

288 echanistic pathway by which Escherichia coli persisters to ofloxacin form in response to a carbon sou

289 acterial stress response pathways that allow persisters to survive many harsh conditions, including a

290 The ability of persisters to survive their interaction with a host is i

291 vest in a slow-growing subpopulation, called persisters, to ensure survival in the face of uncertaint

292 Persister tolerance is generally attributed to minimally

293 due to subpopulation of persistent bacteria (persisters) tolerant to high concentrations of antibioti

294 Drug-tolerant "persister" tumor cells underlie emergence of drug-resist

295 Here we demonstrate that bacterial persisters, under beta-lactam antibiotic treatment, show

296 dentified chromatin regulators essential for persister viability, including BRD4.

297 f azlocillin and cefotaxime on drug-tolerant persisters were done by semisolid plating method.

298 ADHD persisters were impaired compared with controls on all c

299 creased prevalence of dormant cells known as persisters, which are characterized by an up-regulation

300 clude phenotypically dormant cells, known as persisters, which are tolerant to many antibiotics and o