ライフサイエンスコーパス: persister

1 ed to antibiotic-tolerant variants known as 'persisters'.

2 y a small population of dormant cells called persisters.

3 ultures, a finding that is characteristic of persisters.

4 ssociated proteins were unique for ofloxacin persisters.

5 ignificantly higher in resolvers compared to persisters.

6 ess the most therapeutic potential to combat persisters.

7 cteriostatic and does not kill drug-tolerant persisters.

8 rrupting a target in dormant cells will kill persisters.

9 nce of high DO yields sufficient ROS to kill persisters.

10 re currently no viable means for eradicating persisters.

11 small population of dormant bacteria called persisters.

12 enterica, also form 100- to 1,000-fold more persisters.

13 detection distinguished ADHD remitters from persisters.

14 Hydrolyzing corrupted tRNA resuscitates persisters.

15 al component TolC, show higher expression in persisters.

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

17 th the selection of phenotypically tolerant "persisters."

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

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

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

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

22 Our results demonstrate that persisters, although dormant, are primed for metabolite

23 tion can be effective in clearing the entire persister and susceptible populations of bacteria.

24 pulation may contain a diverse collection of persisters and discuss engineering strategies for persis

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

26 ether, these findings suggest a link between persisters and recalcitrance of CF infection and identif

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

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

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

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

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

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

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

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

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

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

37 Persisters are associated with chronic infections and an

38 Although persisters are believed to contribute to difficulties in

39 We find that persisters are distinct from the larger antibiotic-susce

40 Persisters are dormant phenotypic variants of bacterial

41 Persisters are dormant variants of regular cells that fo

42 Persisters are in a dormant metabolic state, even while

43 Persisters are metabolically dormant, so they are highly

44 Persisters are multidrug-tolerant bacteria that could ac

45 The persisters are not drug-resistant mutants and it is uncl

46 s, although the nature and location of these persisters are not known.

47 The surviving persisters are not the result of genetic changes but rep

48 Persisters are phenotypic variants of normal cells and p

49 Persisters are phenotypic variants of regular cells that

50 Persisters are phenotypic variants of the wild type and

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 Bacterial persisters are thought to underlie the relapse of chroni

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

58 esults suggest that, in vivo, RelE-generated persisters are unlikely to play a significant role in th

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

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

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

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

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

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

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

66 n Escherichia coli an increased frequency of persisters, called "high persistence," is conferred by m

67 Microbial persisters can cause recurrent or intractable infections

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

83 The persister cell pool constitutes a reservoir from which d

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

85 erichia coli is involved in the formation of persister cell subpopulations, suggests persistence as a

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

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

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

89 The phenomenon of persister cells and models of Salmonella enterica serova

90 Persister cells are a multi-drug tolerant subpopulation

91 Thus persister cells are a promising target for developing mo

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

93 Bacterial persister cells are highly tolerant to antibiotics and c

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

95 usceptibility of Pseudomonas aeruginosa PAO1 persister cells at growth non-inhibitory concentrations.

96 Bacterial persister cells constitute a small portion of a culture

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

98 Whether persister cells develop through interactions with toxin/

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

100 ions, it serves as a framework for including persister cells in a spatially dependent biofilm model.

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

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

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

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

105 optimal rate of switching between normal and persister cells is found to depend strongly on the frequ

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

107 t antibiotic tolerance of P. aeruginosa PAO1 persister cells is not through QS inhibition and may inv

108 However, control of persister cells is still an unmet challenge.

109 existence of a small fraction of specialized persister cells may be responsible for this tolerance.

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

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

112 Although persister cells seem to exist in planktonic bacterial po

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

114 Persister cells survive antibiotic and other environment

115 antly smaller fraction of multidrug-tolerant persister cells than cultures of Escherichia coli or Sta

116 Bacterial populations produce dormant persister cells that are resistant to killing by all ant

117 Dormant persister cells that are tolerant to killing by antibiot

118 Bacteria are well known to form dormant persister cells that are tolerant to most antibiotics.

119 Targeting persister cells therefore presents a therapeutic opportu

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

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

122 BF8 can sensitize P. aeruginosa persister cells to antibiotics.

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

124 ction offered by the polymeric matrix allows persister cells to evade elimination and serve as a sour

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

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

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

128 ATP levels induces the formation of dormant persister cells which can eventually form biofilms.

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

130 pecially biofilms, produce a small number of persister cells, a genetically identical subpopulation o

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

132 he killing of antibiotic-resistant bacteria, persister cells, and biofilm cells, reduce the number of

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

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

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

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

137 gy to rapidly purify ribosome complexes from persister cells.

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

139 osomal RNA and protein components from these persister cells.

140 as been described for Pseudomonas aeruginosa persister cells.

141 sa produce increased levels of drug-tolerant persister cells.

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

143 death and production of antibiotic-tolerant persister cells.

144 ntifying drugs that eliminate drug-tolerant "persister" cells (infectious disease) or tumor-initiatin

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

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

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

148 Bacterial populations contain persisters, cells which survive exposure to bactericidal

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

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

151 Persister control by BF8 was found to be effective again

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

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

154 Persisters do not have a genetic resistance mechanism, a

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

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

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

158 pe hipA gene to generate a high frequency of persisters, equal to that conferred by the hipA7 allele,

159 sters and discuss engineering strategies for persister eradication.

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

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

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

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

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

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

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

167 Although persisters form during normal growth from native stresse

168 uction but decreased when the pinched cocci (persister) form became the major morphotype.

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

170 Increased persister formation appears to be their sole mechanism f

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

172 iseases, the underlying mechanisms affecting persister formation are not well understood.

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

174 nts employ sophisticated strategies, such as persister formation for rhizobia and reversal of spore g

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

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

177 Toxin/antitoxin (TA) modules are involved in persister formation in Escherichia coli.

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

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

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

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

182 ynamics by considering adaptive response and persister formation separately.

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

184 We find that extending the model of persister formation to include the toxin/antitoxin inter

185 lations of Escherichia coli the frequency of persister formation usually is 10(-7) to 10(-5).

186 Increased persister formation was observed in exponential phase, s

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

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

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

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

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

192 titoxin modules contributed to intracellular persister formation.

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

194 the potential to prevent drug tolerance and persister formation.

195 s responses may act as general activators of persister formation.

196 eads to overexpression of the TisB toxin and persister formation.

197 previously in analysis of a generic model of persister formation.

198 ein kinase activity of HipA is essential for persister formation.

199 ed inhibition of cell growth and increase in persister formation.

200 thereby inhibiting translation and promoting persister formation.

201 strain but did not affect the high levels of persisters formed by the 96-month isolate.

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

203 We find that the persister fraction of the population as a function of wa

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

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

206 rates, we show how fitness loss due to slow persister growth pays off as a risk-reducing strategy.

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

208 Since characterization of persisters has been performed mainly in Escherichia coli

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

210 Persisters have been hypothesized to underlie the recalc

211 Bacterial persisters have been implicated in biofilms and in chron

212 Persisters have traditionally been thought of as metabol

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

214 sociated with generating multidrug-tolerant "persisters." Here we show that unlike persisters of E. c

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

216 his suggests that the late isolate is a high-persister (hip) mutant.

217 High persister (hip) mutants of Pseudomonas aeruginosa are se

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

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

220 n to enhance the generation of drug-tolerant persisters in a process dependent on Lon protease and Re

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

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

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

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

225 n with glpD deleted had a decreased level of persisters in the stationary state.

226 a renewed interest in the role of bacterial persisters in treatment failure in light of a wealth of

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

228 t libraries has not produced mutants lacking persisters, indicating that dormancy mechanisms are redu

229 most highly up-regulated in Escherichia coli persisters is mqsR, a ribonuclease toxin that, along wit

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

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

232 age 96 months) showed a 100-fold increase in persister levels.

233 These observations suggest that persisters may be the main culprit responsible for the r

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

235 Persisters may play a similarly critical role in the rec

236 Proteins required for maintaining persisters may represent realistic targets for discovery

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

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

239 tion and identify an overlooked culprit-high-persister mutants producing elevated levels of drug-tole

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

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

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

243 ctone 3-OC12-HSL significantly increased the persister numbers in logarithmic P. aeruginosa PAO1 or P

244 or Staphylococcus aureus, they can increase persister numbers in response to quorum-sensing-related

245 erant "persisters." Here we show that unlike persisters of E. coli, persisters of Mycobacterium tuber

246 e we show that unlike persisters of E. coli, persisters of Mycobacterium tuberculosis selected with o

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

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

249 hat nutrient stress can select a V. cholerae persister phenotype in environmental reservoirs, with th

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

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

252 omoted a shift to what we have defined as a "persister" phenotype (PP) which was culturable for >700

253 stress, some species of bacteria shift to a "persister" phenotype.

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

255 Knowledge of persister physiology would illuminate avenues for therap

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

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

258 es maintained at high DO levels, rescues the persister population.

259 cycling pathway, successfully eradicates the persister population.

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

261 A clone with increased persister production was isolated and was found to overe

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

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

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

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

266 Some persisters resumed intracellular growth after phagocytos

267 in had no discernible effect on the level of persisters seen in rifampin-treated mice.

268 t samples reported to date: are they spores, persisters, sessile vegetative cells or do they make up

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

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

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

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

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

274 We now show that the small persister subpopulation within a larger antibiotic-susce

275 (TA) modules, have the ability to form more persisters, suggesting a specific role for these toxins

276 e concentration of ROS, thereby facilitating persister survival, and maintenance of high DO yields su

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

278 s a state in which a subpopulation of cells (persisters) survives antibiotic treatment, and has been

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

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

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

282 blishes a strategy for eradicating bacterial persisters that is based on metabolism, and highlights t

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

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

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

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

287 hat stimulating ROS production can eradicate persisters, thus providing a potential strategy to manag

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

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

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

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

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

293 which a sub-population of dormant cells, or 'persisters', tolerates antibiotic treatment.

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

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

296 ADHD persisters were impaired compared with controls on all c

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

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

299 i) and Gram-positive (Staphylococcus aureus) persisters with aminoglycosides.

300 olerant subpopulation of cells, often called persisters, within populations of Mycobacterium smegmati