ライフサイエンスコーパス: aeruginosa

1 ents to the major human pathogen Pseudomonas aeruginosa.

2 ate metabolism and bacterial virulence in P. aeruginosa.

3 and MvaU may contribute to the growth of P. aeruginosa.

4 mens for infections due to drug-resistant P. aeruginosa.

5 ) affords broad coverage against Pseudomonas aeruginosa.

6 helial cells and cocultures with Pseudomonas aeruginosa.

7 pportunistic pathogens including Pseudomonas aeruginosa.

8 F clinical isolates of B. cenocepacia and P. aeruginosa.

9 tains activity against resistant Pseudomonas aeruginosa.

10 smed2 domain of the sensor kinase RetS in P. aeruginosa.

11 f effective strategies to target Pseudomonas aeruginosa.

12 vents T6SS-dependent bacterial killing by P. aeruginosa.

13 n and anthranilate metabolism in Pseudomonas aeruginosa.

14 for phagocytic recognition and uptake of P. aeruginosa.

15 annii, Klebsiella pneumoniae and Pseudomonas aeruginosa.

16 t acinetobacter species, and MDR Pseudomonas aeruginosa.

17 reatment of infections caused by Pseudomonas aeruginosa.

18 agulase-negative staphylococci (21%), and P. aeruginosa (16%), 394 (24%) received IEAT despite IDSA r

19 Staphylococcus aureus (34%) and Pseudomonas aeruginosa (17%), whereas blood cultures most commonly g

20 lebsiella pneumoniae (25.6%) and Pseudomonas aeruginosa (18.9%).

21 r Enterobacteriaceae (76.4 vs. 32.9%) and P. aeruginosa (25.6 vs. 0.3%).

22 2015/16, was for MRSA (97%), followed by P. aeruginosa (81%), S. aureus (79%) and Candida spp (72%),

23 liver transplant recipients, and Pseudomonas aeruginosa (9%) in lung transplant recipients.

24 bles efficient recombineering in Pseudomonas aeruginosa, a concerning human pathogen.

25 Pseudomonas aeruginosa, a Gram-negative bacterium that commonly colo

26 ey mechanism for host control of Pseudomonas aeruginosa, a motile Gram-negative, opportunistic bacter

27 he seven B3-like phages in strain Ps33 of P. aeruginosa, a novel clinical isolate, and assayed the ex

28 In P. aeruginosa, a primary mechanism for protection from redo

29 Emerging evidence suggests the Pseudomonas aeruginosa accessory genome is enriched with uncharacter

30 s suggest certain mutations that arise as P. aeruginosa adapts to the CF lung abrogate T6SS activity,

31 onclude that active cellular processes by P. aeruginosa afford a significant benefit to S. maltophili

32 Higher rates of resistant P. aeruginosa after patients were treated with carbapenems,

33 aracterized in the regulation of Pseudomonas aeruginosa alginate biosynthesis(3,4), as a regulator of

34 us and 16- to 64-fold against E. coli and P. aeruginosa alongside reduced cytotoxicity.

35 B1 NDM-1 and VIM-2 MBLs, and the class C P. aeruginosa AmpC.

36 es a decrease in the activity of ClpXP in P. aeruginosa, an effect which was also achieved by the tre

37 Multiple clinical isolates of Pseudomonas aeruginosa, an important human pathogen, have naturally

38 d identified 11 cyanopeptides in Microcystis aeruginosa and 17 in Dolichospermum flos-aquae.

39 nteractions between a bacterium, Pseudomonas aeruginosa and a yeast, Candida albicans, induce the res

40 acteria, including the pathogens Pseudomonas aeruginosa and Acinetobacter baumannii.

41 Only P. aeruginosa and Aspergillus were associated with progress

42 Both P. aeruginosa and Bcc use type VI secretion systems (T6SSs)

43 Pseudomonas aeruginosa and Burkholderia cepacia complex (Bcc) specie

44 ics against carbapenem-resistant Pseudomonas aeruginosa and carbapenem-resistant Enterobacteriaceae.

45 patients with positive blood cultures for P. aeruginosa and Escherichia coli, respectively.

46 ), which is higher than that of wild-type P. aeruginosa and even the strongly electrogenic organism,

47 toward both Gram stain-negative Pseudomonas aeruginosa and Gram stain-positive Staphylococcus aureus

48 at UQ(9) is the major quinone of Pseudomonas aeruginosa and is required for growth under anaerobic re

49 he CF lung abrogate T6SS activity, making P. aeruginosa and its human host susceptible to potentially

50 ere found to have evolved specifically in P. aeruginosa and nearly each species carries different reg

51 P. aeruginosa and OPP-C mean log(10) CFU/cm(2) counts were

52 P. aeruginosa and OPP-C mean log(10) CFU/ml counts were als

53 and 3.87 +/- 0.78 vs. 3.21 +/- 1.11) for P. aeruginosa and OPP-C, respectively.

54 and 5.27 +/- 1.10 vs. 4.74 +/- 1.06) for P. aeruginosa and OPP-C, respectively.

55 c biology constructs to identify genes in P. aeruginosa and other organisms that enhance electrogenic

56 e and severe pneumonia caused by Pseudomonas aeruginosa and poor wound healing.

57 e, particularly in tuberculosis, leprosy, P. aeruginosa and S. aureus infections, where it develops v

58 Both P. aeruginosa and S. aureus require iron to infect the mamm

59 tosed inhaled bacterial pathogens such as P. aeruginosa and S. aureus, cloaking the bacteria from neu

60 Pseudomonas aeruginosa and Staphylococcus aureus are opportunistic b

61 y using both model membranes and Pseudomonas aeruginosa and Staphylococcus aureus, representing Gram-

62 a enteritidis, Listeria innocua, Pseudomonas aeruginosa and Streptococcus pneumoniae did not interfer

63 fosfomycin susceptibility testing against P. aeruginosa and stress the need for P. aeruginosa-specifi

64 heme release, signaling, and transport in P. aeruginosa and suggest a functional link between the ECF

65 tions are presumed to be a "dead-end" for P. aeruginosa and to have no impact on transmission.

66 gainst Staphylococcus aureus and Pseudomonas aeruginosa and with their geographical origin.

67 e, antibiogram of Pseudomonas aeruginosa (P. aeruginosa), and the distribution of virulence genes (op

68 g 288 Staphylococcus aureus, 456 Pseudomonas aeruginosa, and 1588 Escherichia coli genomes.

69 sceptibility testing of Enterobacterales, P. aeruginosa, and A. baumannii complex isolates with limit

70 et results for Enterobacterales, Pseudomonas aeruginosa, and Acinetobacter baumannii complex for pati

71 fluenzae, Staphylococcus aureus, Pseudomonas aeruginosa, and Aspergillus infections were all associat

72 y against Staphylococcus aureus, Pseudomonas aeruginosa, and Enterococcus faecalis although PSO had a

73 hogenic Escherichia coli (UPEC), Pseudomonas aeruginosa, and Staphylococcus aureus, with up to 3.7 lo

74 umoniae, Acinetobacter baumanii, Pseudomonas aeruginosa, and Staphylococcus aureus.

75 ica, Mycobacterium tuberculosis, Pseudomonas aeruginosa, and Staphylococcus aureus.

76 ed for growth arrest survival of Pseudomonas aeruginosa, and that this requirement is independent of

77 3.3%, and 89.2% for the Enterobacterales, P. aeruginosa, and the A. baumannii complex, respectively.

78 ilia formed well-integrated biofilms with P. aeruginosa, and these organisms colocalize in the lung d

79 uman pathogens Escherichia coli, Pseudomonas aeruginosa, and Vibrio cholerae, and the plant pathogen

80 analysis of the QS-mediated response of a P. aeruginosa antibiotic resistant mutant that overexpresse

81 Chronic infections by Pseudomonas aeruginosa are characterized by biofilm formation, which

82 Pyocins, bacteriocins of P. aeruginosa, are potent and diverse protein antibiotics t

83 protein family member, PscK from Pseudomonas aeruginosa, as well as the structure of its interacting

84 geted fashion while in contrast, Pseudomonas aeruginosa assembles and fires its T6SS apparatus only a

85 e optimal antibiotic regimen for Pseudomonas aeruginosa bacteremia is controversial.

86 re-associated infections such as Pseudomonas aeruginosa bacteremia pose a major clinical risk for hos

87 including 767 hospitalized patients with P. aeruginosa bacteremia treated with beta-lactam monothera

88 lin-tazobactam as definitive treatment of P. aeruginosa bacteremia.

89 compromises clearance of wound-colonizing P. aeruginosa bacteria and exacerbates infection-induced mo

90 aeruginosa population and required viable P. aeruginosa bacteria.

91 e results shed light on how mucus impacts P. aeruginosa behavior, and may inspire novel approaches fo

92 sample (>90% water) of a mature Pseudomonas aeruginosa biofilm in its native state.

93 As an example, Pseudomonas aeruginosa biofilm is grown from single cells, and it is

94 was proposed for the imaging of Pseudomonas aeruginosa biofilms on metallic surfaces using an infrar

95 to the structure and function of Pseudomonas aeruginosa biofilms.

96 quantify the virulence of 100 individual P. aeruginosa bloodstream isolates and performed whole-geno

97 dinately as global repressors in Pseudomonas aeruginosa by binding to AT-rich regions of the chromoso

98 erties, is not upregulated in response to P. aeruginosa by cystic fibrosis airway epithelia.

99 teins promote uptake, but not binding, of P. aeruginosa by murine neutrophils, which supports a role

100 immunity nucleases of its host, Pseudomonas aeruginosa, by constructing a proteinaceous nucleus-like

101 Methicillin-resistant S. aureus, P. aeruginosa, C. difficile, and fungal infections all had

102 While P. aeruginosa can initiate long-term infections in younger

103 use a mouse infection model to show that P. aeruginosa can spread from the bloodstream to the gallbl

104 Pseudomonas aeruginosa causes severe multidrug-resistant infections

105 Overall, our findings indicate that this P. aeruginosa CDI system functions as both an interbacteria

106 we analysed the transcriptomic profile of P. aeruginosa cells isolated from lungs of infected mice an

107 Although early P. aeruginosa CF infection is thought to reflect acquisitio

108 ation after intratracheal LPS or Pseudomonas aeruginosa challenge.

109 mice after intratracheal LPS or Pseudomonas aeruginosa challenge.

110 nstruct a novel SDS biosensor in Pseudomonas aeruginosa chassis.

111 aeruginosa The challenge set included 123 P. aeruginosa clinical isolates from 12 countries.

112 ge (e.g., Staphylococcus aureus, Pseudomonas aeruginosa, Clostridium difficile, and fungal infections

113 nemase families from Enterobacterales and P. aeruginosa colonies on commonly used agar media.

114 mise of Scnn1b-Tg mice as models of early P. aeruginosa colonization in the CF lung.

115 ing polymicrobial infection with Pseudomonas aeruginosa Colonization, persistence, and virulence of S

116 Pseudomonas aeruginosa colonizing airways is consistently exposed to

117 eria, the opportunistic pathogen Pseudomonas aeruginosa contains two ClpP homologs: ClpP1 and ClpP2.

118 ucers among carbapenem-resistant Pseudomonas aeruginosa (CRPA) isolates warrants an expansion of dete

119 VI secretion system locus II (H2-T6SS) of P. aeruginosa delivers AmpDh3 (but not AmpD or AmpDh2) to t

120 n together, our observations suggest that P. aeruginosa deploys a virulence mechanism to induce ribos

121 at interfere specifically with late-stage P. aeruginosa development.

122 stion, we purified a five-member Pseudomonas aeruginosa division complex consisting of FtsQLB-FtsWI.

123 fmRS may contribute to host adaptation by P. aeruginosa during chronic infections.

124 mentary data regarding the role of GSH in P. aeruginosa during mammalian infection.

125 es, Acinetobacter baumannii, and Pseudomonas aeruginosa during susceptibility testing.

126 It has been shown that Pseudomonas aeruginosa elastase (LasB) and Clostridium histolyticum

127 Importantly, polymicrobial infection with P. aeruginosa elicited significantly higher S. maltophilia

128 f the order Enterobacterales and Pseudomonas aeruginosa, enriched for drug resistance.

129 nt risk factors for mortality in Pseudomonas aeruginosa episodes.

130 Pseudomonas aeruginosa exhibits a high requirement for iron, which i

131 a hexasaccharide fragment of the Pseudomonas aeruginosa exopolysaccharide Pel was assembled using a [

132 In Pseudomonas aeruginosa, expression of the T3SS is regulated by a sig

133 n the rates of ESBL, CRE and MDR Pseudomonas aeruginosa following ASP.

134 Furthermore, we show that heme protects P. aeruginosa from CP-mediated inhibition of iron uptake an

135 es of the opportunistic pathogen Pseudomonas aeruginosa from patients with cystic fibrosis (CF) frequ

136 ureus, a common pathogen co-isolated with P. aeruginosa from polymicrobial human infections.

137 the gallbladder is crucial for spread of P. aeruginosa from the bloodstream to the feces during bact

138 d site, which was exploited to reduce the P. aeruginosa genome by 837 kb (13.5%).

139 The P. aeruginosa genome encodes two heme uptake systems, the h

140 We searched P. aeruginosa genomes from collections available from sever

141 We used a diverse set of 58 complete P. aeruginosa genomes to curate a set of 4,440 core genes f

142 a valuable tool for the rapid analysis of P. aeruginosa genomes.

143 The human pathogen Pseudomonas aeruginosa harbors three paralogous zinc proteases annot

144 P. aeruginosa harbours hundreds of regulatory genes that pl

145 In particular, electrogenic Pseudomonas aeruginosa has been studied with the utility of its comp

146 IGPS from Pseudomonas aeruginosa has the highest turnover number of all charac

147 nscripts as they are being synthesized in P. aeruginosa, identify the transcripts targeted by RsmA, a

148 Our structure of P. aeruginosa IGPS has eight molecules in the asymmetric un

149 Here, we present the crystal structure of P. aeruginosa IGPS in complex with reduced CdRP, a nonreact

150 nserved active-site residues, Phe(201) in P. aeruginosa IGPS, is by mutagenesis demonstrated to be im

151 pe of exclusion mediated by a prophage in P. aeruginosa IMPORTANCE Pseudomonas aeruginosa is a Gram-n

152 thereby providing a growth advantage for P. aeruginosa in bacterial competition.

153 us at killing the model organism Pseudomonas aeruginosa in biofilms and in a murine chronic lung infe

154 y increased killing of B. cenocepacia and P. aeruginosa in CF MDMs in a dose-dependent manner.

155 g from injury upon intratracheal Pseudomonas aeruginosa in mice.

156 P aeruginosa increased N-WASP-Y256 phosphorylation, which

157 A from other bacterial species, ZapA from P. aeruginosa induced PaFtsZ protofilaments to associate in

158 F overexpression blocked N-WASP effects in P aeruginosa-induced actin stress fiber formation and incr

159 ated that N-WASP downregulation attenuated P aeruginosa-induced actin stress fiber formation and prev

160 osine levels and significantly attenuated P. aeruginosa-induced acute lung injury, as assessed by lun

161 lly, inhibition of inflammasome prevented P. aeruginosa-induced acute lung injury.

162 suggesting a role for N-WASP in promoting P aeruginosa-induced adherens junction rupture.

163 P aeruginosa-induced dissociation between VE-cadherin and

164 trategies for prevention and treatment of P. aeruginosa-induced pneumonia and subsequent ARDS.

165 The mechanisms underlying P aeruginosa-induced vascular permeability are not well un

166 n (from 3.33 to 2.47 per 10,000), and MDR P. aeruginosa infection (from 13.10 to 9.43 per 10,000), wi

167 ted that the oxygen levels at the site of P. aeruginosa infection can strongly influence virulence an

168 BPI) is strongly associated with Pseudomonas aeruginosa infection in cystic fibrosis (CF), non-CF bro

169 Conversely, T3SS-incompetent P aeruginosa infection produced non-cytotoxic amyloids wit

170 edominant virulence genes associated with P. aeruginosa infection.

171 rk that has advanced our understanding of P. aeruginosa infection.

172 Pseudomonas aeruginosa infections are increasingly multidrug resista

173 at phagocytes are crucial for controlling P. aeruginosa infections, our data suggest that feedback in

174 get for antibiotics development to manage P. aeruginosa infections.

175 ins or aminoglycosides for drug-resistant P. aeruginosa infections.

176 inspire novel approaches for controlling P. aeruginosa infections.

177 hage in P. aeruginosa IMPORTANCE Pseudomonas aeruginosa is a Gram-negative bacterium frequently isola

178 The opportunistic pathogen Pseudomonas aeruginosa is a leading cause of morbidity and mortality

179 The opportunistic pathogen Pseudomonas aeruginosa is a major cause of antibiotic-tolerant infec

180 In conclusion, P. aeruginosa is a major pathogen of O. niloticus and C. ga

181 Pseudomonas aeruginosa is a priority pathogen for the development of

182 Pseudomonas aeruginosa is an extracellular opportunistic bacterial p

183 Pseudomonas aeruginosa is an opportunistic human pathogen that frequ

184 Pseudomonas aeruginosa is an opportunistic pathogen that senses and

185 Since the denitrification metabolism of P. aeruginosa is believed to be important for the pathogeni

186 evalence of carbapenem-resistant Pseudomonas aeruginosa is increasing.

187 The opportunistic pathogen Pseudomonas aeruginosa is responsible for much of the morbidity and

188 Prior work has shown that P. aeruginosa is starved of iron in the presence of CP.

189 M) against a large collection of clinical P. aeruginosa isolates (n = 103) to provide clinicians a ph

190 The 28 patients had P. aeruginosa isolates available both before and after TOL-

191 Here, we show P. aeruginosa isolates from teenage and adult CF patients,

192 The genomes of susceptible P. aeruginosa isolates harbor T6SS-abrogating mutations, th

193 tients infected with carbapenem-resistant P. aeruginosa isolates susceptible to TOL-TAZ and treated w

194 able platform for the rapid comparison of P. aeruginosa isolates using whole-genome sequencing (WGS)

195 Also, 46.2% of Pseudomonas aeruginosa isolates were carbapenem-resistant preimpleme

196 , where 309 Enterobacterales and Pseudomonas aeruginosa isolates were evaluated by NG-Test Carba 5 (N

197 Fourteen patients (50%) had P. aeruginosa isolates which developed high-level TOL-TAZ r

198 We previously identified Pseudomonas aeruginosa isolates with characteristics typical of chro

199 zidime-avibactam (CAZ-AVI) had subsequent P. aeruginosa isolates with high-level resistance to CAZ-AV

200 Among the P. aeruginosa isolates, 2 (6.9%) VMEs and 3 (3.3%) MEs were

201 ates of the Enterobacterales, 50 Pseudomonas aeruginosa isolates, and 50 Acinetobacter species isolat

202 5 Enterobacterales isolates, 119 Pseudomonas aeruginosa isolates, and 83 Acinetobacter baumannii comp

203 DI) system enriched among highly virulent P. aeruginosa isolates.

204 ronmental opportunistic pathogen Pseudomonas aeruginosa, it has been shown that overexpression of dif

205 el to elucidate PelX function as Pseudomonas aeruginosa lacks a pelX homologue in its pel gene cluste

206 (a role often facilitated by CheC, which P. aeruginosa lacks).

207 he historic phage B3 that infect Pseudomonas aeruginosa Like other phage groups, the B3-like group co

208 Pseudomonas aeruginosa, like many bacilliforms, are not limited only

209 tructures of inhibitors bound to Pseudomonas aeruginosa LpxC as guides, resulted in the discovery of

210 ts of ClpXP on the quorum sensing (QS) of P. aeruginosa, mainly by degrading proteins (e.g., PhnA, Ph

211 owed bactericidal effect against Pseudomonas aeruginosa, making PA the most susceptible of the strain

212 In this study, we created a P. aeruginosa mutant defective in GSH biosynthesis to exami

213 rodentium, Escherichia coli, or Pseudomonas aeruginosa mutant strain DeltapopB Moreover, BMDMs defic

214 From 95 isogenic P. aeruginosa mutant, an hmgA mutant generated the highest

215 ity of hundreds of genetically engineered P. aeruginosa mutants is needed.

216 Enterobacterales and lowest for Pseudomonas aeruginosa Nevertheless, even for Enterobacterales, ther

217 nd production of microcystins in Microcystis aeruginosa NIES-843.

218 A single P. aeruginosa non-coding RNA, P11, is both necessary and su

219 trisaccharide repeating unit of Pseudomonas aeruginosa O11 via a highly stereoselective and efficien

220 re-dependent methods to quantify Pseudomonas aeruginosa, opportunistic pathogens capable of growth on

221 but did not inhibit biofilms by Pseudomonas aeruginosa or Bacillus subtilis, and inhibited biofilms

222 Isolates from each medium identified as P. aeruginosa or Enterobacteriaceae were tested for suscept

223 During infection of a host, Pseudomonas aeruginosa orchestrates global gene expression to adapt

224 e the prevalence, antibiogram of Pseudomonas aeruginosa (P. aeruginosa), and the distribution of viru

225 analyses based on lung function, Pseudomonas aeruginosa (PA) status, and follow-up time intervals wer

226 in-resistant Enterococcus (VRE), Pseudomonas aeruginosa (PA), and Candida albicans (CA)].

227 including the common CF pathogen Pseudomonas aeruginosa (Pa).

228 herichia coli (Ec, m/z 1797) and Pseudomonas aeruginosa (Pa, m/z 1446) using on-tissue acid hydrolysi

229 chemical properties of FtsZ from Pseudomonas aeruginosa (PaFtsZ) and the effects of its two positive

230 Here, we report that P. aeruginosa PAO1 produced sulfane sulfur, including gluta

231 Pseudomonas aeruginosa pneumonia elicits endothelial cell release of

232 and improved survival in a mouse model of P aeruginosa pneumonia.

233 rectly correlated with the density of the P. aeruginosa population and required viable P. aeruginosa

234 P aeruginosa possessing a functional T3SS and effectors in

235 These findings demonstrate that P. aeruginosa QS molecules may confer protection to neighbo

236 9 days and 147 days against S. aureus and P. aeruginosa, respectively, compared to 70 days of activit

237 from Salmonella Typhimurium and Pseudomonas aeruginosa, respectively, reveals that Eag chaperones mi

238 In the opportunistic pathogen Pseudomonas aeruginosa, RsmA is an RNA-binding protein that plays cr

239 se model of subcutaneous inoculation with P. aeruginosa, rTCP96 reduced bacterial levels.

240 tomic, and proteomic analyses reveal that P. aeruginosa's main QS molecule, N-(3-Oxododecanoyl)-L-hom

241 by a small subset of globally distributed P. aeruginosa sequence types (STs), termed "high-risk clone

242 creted phospholipase effector of Pseudomonas aeruginosa, serves as a prototype to model large, dynami

243 till present in Vibrio cholerae, Pseudomonas aeruginosa, Shewanella oneidensis and Methylomicrobium a

244 These were both SARS-CoV-2 and P. aeruginosa specific, and bystander activated, which may

245 nst P. aeruginosa and stress the need for P. aeruginosa-specific breakpoints.

246 nesis can also trigger T6SS activation in P. aeruginosa Specifically, we developed a CRISPR interfere

247 gainst many pathogens, including Pseudomonas aeruginosa, Staphylococcus aureus, and Escherichia coli

248 wild-type littermates with the laboratory P. aeruginosa strain PAO1 and CF clinical isolates and then

249 Our objective was to define the extent of P. aeruginosa strain sharing in early CF infections and its

250 ested against colistin-resistant Pseudomonas aeruginosa strains including clinical isolates to exploi

251 r, seven of eight Bcc strains outcompeted P. aeruginosa strains isolated from the same patients.

252 illin, and tetracycline, highlighting MDR P. aeruginosa strains of potential public health concern.

253 Pseudomonas aeruginosa strains with loss-of-function mutations in th

254 MDR efflux systems can be understood as a P. aeruginosa strategy to keep the robustness of the QS reg

255 including Bacillus subtilis and Pseudomonas aeruginosa strongly alter the collective dynamics due to

256 e characterization of ErfA regulon across P. aeruginosa subfamilies revealed a second conserved targe

257 d with chronic respiratory infection with P. aeruginosa, suggesting that either the chronicity or the

258 show that the ClpXP protease of Pseudomonas aeruginosa suppresses its antimicrobial activity against

259 ceptible" at breakpoint; and (4) Pseudomonas aeruginosa that merely lack porin OprD?

260 G (Carba-R NxG) in a global collection of P. aeruginosa The challenge set included 123 P. aeruginosa

261 se and serine-carbapenemase production in P. aeruginosa The mCIM test was performed according to Clin

262 terobacterales, whereas it was 96.0% with P. aeruginosa The MCR-1 LFA and EDTA-CBDE methods are both

263 ence of de-N-acetylated muropeptides from P. aeruginosa The method developed here offers a robust and

264 tic-resistant bacteria (MRSA and Pseudomonas aeruginosa), the most common cause of biomaterial implan

265 In the case of P. aeruginosa, the effector protein ExoS is central to limi

266 ly inhibits biofilm formation in Pseudomonas aeruginosa, the most widely used model for serious biofi

267 he infection of Caenorhabditis elegans by P. aeruginosa, the precise pathways and mechanism(s) of tra

268 In Pseudomonas aeruginosa, the transition between planktonic and biofil

269 with 110 isolates of Enterobacterales and P. aeruginosa These results were compared to the expected g

270 d that this association is not limited to P. aeruginosa This is to be contrasted with chronic respira

271 a similar remodeling of the BfmRS TCS in P. aeruginosa This study highlights the plasticity of TCSs

272 oY contributes to the virulence arsenal of P aeruginosa through the subversion of endothelial amyloid

273 er membrane perturbation can be sensed by P. aeruginosa to activate the T6SS even when the disruption

274 a suggest that feedback inhibition allows P. aeruginosa to direct its effector arsenal against the ce

275 nts with at least a four-fold increase in P. aeruginosa TOL-TAZ MICs after exposure to TOL-TAZ.

276 P. aeruginosa Type I-C Cascade-Cas3 (PaeCas3c) facilitates

277 anscription activation domain to Pseudomonas aeruginosa type I-F Cas proteins, we activate gene trans

278 tor of the expression and activity of the P. aeruginosa Type I-F CRISPR-Cas system.

279 We report that P. aeruginosa upregulates expression of heme uptake machine

280 Pseudomonas aeruginosa uses a type III secretion system (T3SS) to in

281 ibition of insects and mammalian hosts by P. aeruginosa utilizes the well-known exotoxin A effector.

282 mine how loss of GSH biosynthesis affects P. aeruginosa virulence.

283 nsively drug-resistant strain of Pseudomonas aeruginosa was detected in a hospital in Madrid, Spain.

284 P. aeruginosa was isolated from 90 examined fish (31.57%),

285 P. aeruginosa was most significantly associated with develo

286 Pseudomonas aeruginosa was the most common CRGNB each year.

287 transcripts that RsmA associates with in P. aeruginosa We also find that the RNA chaperone Hfq targe

288 planktonic- and biofilm-cultured Pseudomonas aeruginosa We identified a core assembly of PG that is p

289 Similarly to P. aeruginosa, we show that heme protects S. aureus from CP

290 s against Enterobacteriaceae and Pseudomonas aeruginosa were identified.

291 Staphylococcus aureus and Pseudomonas aeruginosa were isolated in 10.5 and 6.4% of the specime

292 The Gram-negative bacteria E. coli and P. aeruginosa were particularly sensitive to aggregation-in

293 bacterial killing curves against Pseudomonas aeruginosa were utilized.

294 KPC-, VIM-, and NDM-producing P. aeruginosa were well defined by the conventional mCIM an

295 lerae can induce T6SS dynamic activity in P. aeruginosa when delivered to or expressed in the peripla

296 Identification of carbapenemase-producing P. aeruginosa will have therapeutic, epidemiological, and i

297 ich was also achieved by the treatment of P. aeruginosa with N-acetylglucosamine (GlcNAc), a widespre

298 e deletions (7-424 kilobases) in Pseudomonas aeruginosa with near-100% efficiency, while Cas9 yielded

299 Isolation of P. aeruginosa with new resistance to antipseudomonal drugs

300 tegories to other organisms like Pseudomonas aeruginosa without supporting evidence.

301 In this manner, P. aeruginosa would impair host translation and block antib