ライフサイエンスコーパス: aeruginosa

1 osed to the toxic cyanobacterium Microcystis aeruginosa.

2 ins of Staphylococcus aureus and Pseudomonas aeruginosa.

3 he opportunistic human pathogen, Pseudomonas aeruginosa.

4 pyochelin siderophore system in Pseudomonas aeruginosa.

5 s in many Enterobacteriaceae and Pseudomonas aeruginosa.

6 ce and the ability to cause bacteremia of P. aeruginosa.

7 listin in vivo against colistin-resistant P. aeruginosa.

8 ra of membrane grown biofilms of Pseudomonas aeruginosa.

9 res of Aspergillus fumigatus and Pseudomonas aeruginosa.

10 e that promotes the opsonophagocytosis of P. aeruginosa.

11 red a novel, targetable defense system in P. aeruginosa.

12 pecies-specific activity against Pseudomonas aeruginosa.

13 ression of genes ftsZ, psbA1, and glmS in M. aeruginosa.

14 illus subtilis and Gram-negative Pseudomonas aeruginosa.

15 ecific IgG1 candidate, targeting Pseudomonas aeruginosa.

16 ntial persistence and virulence factor in P. aeruginosa.

17 t is considered inactive against Pseudomonas aeruginosa.

18 pressed in the outer membrane of Pseudomonas aeruginosa.

19 rectly contribute to its activity against P. aeruginosa.

20 tained when tested on pathogenic Pseudomonas aeruginosa.

21 lysis for the bacterial pathogen Pseudomonas aeruginosa.

22 taphylococcus aureus (12.9%) and Pseudomonas aeruginosa (11.5%) were the most common pathogens implic

23 ority of Gram negative bacteria (Pseudomonas aeruginosa, 16-32 mug/mL, Klebsiella pneumoniae > 32 mug

24 hest in Acinetobacter species (71.9%) and P. aeruginosa (23.6%).

25 ilution (BMD) for 99 isolates of Pseudomonas aeruginosa, 26 Acinetobacter baumannii isolates, and 11

26 Klebsiella pneumoniae (37%) and Pseudomonas aeruginosa (30%); 28% were ceftazidime-non-susceptible.

27 a microchip for rapid (<1h) detection of P. aeruginosa (6294), S. aureus(LAC), through on-chip elect

28 ococcus aureus and gram-negative Pseudomonas aeruginosa (99.3 +/- 1.9% and 88.5 +/- 3.3% respectively

29 The CA values for P. aeruginosa, A. baumannii, and S. maltophilia were 94.1%,

30 The essential agreement values for P. aeruginosa, A. baumannii, and S. maltophilia were 99.5%,

31 iously problematic in hospitals: Pseudomonas aeruginosa, Acinetobacter baumannii, and Staphylococcus

32 negative opportunistic pathogen, Pseudomonas aeruginosa Activation of phospholipase activity is induc

33 P. aeruginosa adhered avidly to lung vasculature, where pat

34 se corneas becomes vulnerable to Pseudomonas aeruginosa adhesion if it lacks the innate defense prote

35 , or TLR9 (-/-), were more susceptible to P. aeruginosa adhesion than wild-type (3.8-fold, 3.6-fold r

36 They also suggest increased P. aeruginosa adhesion to MyD88(-/-) and blotted corneas is

37 However, P. aeruginosa airway infection persisted.

38 Administration of the flavonoids to P. aeruginosa alters transcription of quorum sensing-contro

39 ion in the pathogenic bacterium, Pseudomonas aeruginosa Although public goods producers were selected

40 imental endocarditis (EE) due to Pseudomonas aeruginosa, an archetype of difficult-to-treat infection

41 CI, 88.2 to 99.9; range, 93.3 to 100) for P. aeruginosa and 18.8% (95% CI, 10.4 to 30.1; range, 8.7 t

42 Thirty P. aeruginosa and 30 A. baumannii isolates previously chara

43 abditis elegans from lethal infections of P. aeruginosa and A. baumannii and enhanced the activity of

44 ore, D-RR4 was more capable of disrupting P. aeruginosa and A. baumannii biofilms when compared to co

45 tection of carbapenemase production among P. aeruginosa and A. baumannii Ten testing sites then evalu

46 ance against two MDR isolates of Pseudomonas aeruginosa and Acinetobacter baumannii through in vitro

47 ative bacilli (CPNFs), including Pseudomonas aeruginosa and Acinetobacter baumannii, is necessary to

48 t multidrug-resistant strains of Pseudomonas aeruginosa and Acinetobacter baumannii.

49 sl and PcrV enhanced neutrophil uptake of P. aeruginosa and also greatly increased inhibition of T3S

50 rug by LPS from F. tularensis vs Pseudomonas aeruginosa and by F. tularensis live bacteria vs the clo

51 tained inhibitory effect on the growth of P. aeruginosa and can reduce the number of viable colonies

52 nes) and gram-negative bacteria (Pseudomonas aeruginosa and Escherichia coli) over time through lag a

53 ed by the opportunistic pathogen Pseudomonas aeruginosa and is an important biofilm constituent criti

54 s for mucin-based nutrient acquisition by P. aeruginosa and reveal a host-pathogen dynamic that may c

55 ironment to modulate interactions between P. aeruginosa and S. aureus We demonstrate that P. aerugino

56 versus antagonistic interactions between P. aeruginosa and S. aureus.

57 thogens that cause the corneal ulcers are P. aeruginosa and S. aureus.

58 icles were much more effective at killing P. aeruginosa and S. epidermidis at basic pH values (pH = 9

59 terior of the filament among B. subtilis, P. aeruginosa and Salmonella enterica.

60 ells (E. coli, B. subtilis, Enterococcus, P. aeruginosa and Salmonella typhi) to antibiotics such as

61 Through our analyses of P. aeruginosa and six Streptococci, we show that ensembles

62 d antibacterial activity against Pseudomonas aeruginosa and Staphylococcus aureus was assessed by mic

63 y of raw rapeseed honeys against Pseudomonas aeruginosa and Staphylococcus aureus, with a particular

64 ata from 28 clinical isolates of Pseudomonas aeruginosa and strains evolved in laboratory experiments

65 tal gene transfer by the species Pseudomonas aeruginosa and subsequently abundant P. aeruginosa clone

66 had over 85% inhibition against growth of P. aeruginosa and ten honey samples against S. aureus.

67 expression of the sRNAs RsmY and RsmZ in P. aeruginosa and the small dual-function regulatory RNA, R

68 teractions with their targets in Pseudomonas aeruginosa and verified the method with a known regulon

69 Here we report the influence of various P. aeruginosa and, for comparison, Escherichia coli LPS env

70 coli, Staphylococcus aureus and Pseudomonas aeruginosa) and in vitro anti-proliferative activity wer

71 ates of Enterobacteriaceae spp., Pseudomonas aeruginosa, and Acinetobacter baumannii chosen to provid

72 odification in Escherichia coli, Pseudomonas aeruginosa, and Bacillus subtilis.

73 tant Acinetobacter baumannii and Pseudomonas aeruginosa, and carbapenem-resistant and third-generatio

74 niae, A cinetobacter baumannii, P seudomonas aeruginosa, and E nterobacter spp. were analyzed by MALD

75 dermidis, Enterococcus faecalis, Pseudomonas aeruginosa, and Klebsiella pneumoniae, which are frequen

76 h we hormone manipulated, inoculated with P. aeruginosa, and then examined for outcomes and inflammat

77 ns by the opportunistic pathogen Pseudomonas aeruginosa are a major cause of mortality in cystic fibr

78 g infection and show that C. albicans and P. aeruginosa are synergistically virulent.

79 ci, Streptococcus pneumoniae and Pseudomonas aeruginosa are the leading isolates in ocular infections

80 Using Pseudomonas aeruginosa as a model system, the authors show that secr

81 owed stronger inhibitory activity against P. aeruginosa associated with plastic compared to 3-D cells

82 DJK-5 exerted potent inhibition of P. aeruginosa association with both substrates, only in ser

83 exhibited more potent ability to inhibit P. aeruginosa association with both substrates.

84 two domains and is able to kill Pseudomonas aeruginosa at sub-micromolar concentrations.

85 ayed acceptable bacterial killing against P. aeruginosa ATCC 27853 and no nephrotoxicity was found af

86 s to assess the applicability of Pseudomonas aeruginosa ATCC9027 and its validated bioluminescent str

87 , with Staphylococcus aureus and Pseudomonas aeruginosa being the two most commonly isolated species.

88 e efficacy of most antimicrobials against P. aeruginosa biofilm formation, which in turn depends on t

89 Pseudomonas aeruginosa biofilm infections are difficult to treat wit

90 ptome map of the mature in vitro Pseudomonas aeruginosa biofilm model, revealing contemporaneous yet

91 ild-type mice were infected with Pseudomonas aeruginosa biofilms and, akin to Nod2(-/-) mice, were fo

92 to shape competitive dynamics in Pseudomonas aeruginosa biofilms.

93 rther pathophysiological understanding of P. aeruginosa biofilms.

94 Moreover, Pseudomonas aeruginosa BioH is more highly expressed than E. coli Bi

95 ted information about the role of PhoQ in P. aeruginosa bloodstream infections.

96 um samples from CF patients infected with P. aeruginosa but not in samples from uninfected patients.

97 , we evaluated inhibition of virulence in P. aeruginosa by a designed peptide (RpoN molecular roadblo

98 describe for the first time how Pseudomonas aeruginosa can utilize human recombinant MIF (rMIF) to s

99 N-acetylglucosaminidase NagZ of Pseudomonas aeruginosa catalyzes the first cytoplasmic step in recyc

100 CF-ALF influences the P. aeruginosa cell wall by reducing the content of one of i

101 ctor PqsR is a necessary component in the P. aeruginosa cell-to-cell signaling network.

102 s cross-species interactions, as Pseudomonas aeruginosa cells also become attracted to the electrical

103 NTD) being imported into FpvAI-expressing P. aeruginosa cells by a process analogous to that used by

104 tely 90% of Escherichia coli and Pseudomonas aeruginosa cells within 90-120 and 5-30 min, respectivel

105 d serious damage and significant lysis to M. aeruginosa cells.

106 tivity in a large collection (n = 333) of P. aeruginosa CF isolates.

107 lation is modulated by IL-1R and Pseudomonas aeruginosa challenge but is insufficient for inhibiting

108 90% for detecting carbapenemase-producing P. aeruginosa Class D carbapenemases were the most prevalen

109 t improved CFTR trafficking could enhance P. aeruginosa clearance from the CF airway by activating PT

110 t improved CFTR trafficking could enhance P. aeruginosa clearance through activating the tumor suppre

111 onas aeruginosa and subsequently abundant P. aeruginosa clone C.

112 sporters that control the Cu(+) levels in P. aeruginosa compartments.

113 ese observations suggest that C. albicans-P. aeruginosa cross talk in vivo can benefit both organisms

114 ce regulator (CFTR) that reduces Pseudomonas aeruginosa culture positivity in CF patients with unclea

115 P. aeruginosa defective in the stringent response also had

116 ruginosa strain, and after the first year P. aeruginosa densities rebounded.

117 caftor caused marked reductions in sputum P. aeruginosa density and airway inflammation and produced

118 oduced rapid decreases in sputum Pseudomonas aeruginosa density that began within 48 hours and contin

119 We found that female mice inoculated with P. aeruginosa died earlier and showed slower bacterial clea

120 ntribution of hepP to the pathogenesis of P. aeruginosa during burn wound infection.

121 ere positively but weakly correlated with P. aeruginosa (E. coli vs P. aeruginosa tau = 0.090, p = 0.

122 gle-dose phage therapy was active against P. aeruginosa EE and highly synergistic with ciprofloxacin.

123 nefarious Gram-negative pathogen Pseudomonas aeruginosa encodes eleven LTs.

124 During infection, P. aeruginosa enters the terminal bronchioles and alveoli a

125 Here, we show that a secreted P. aeruginosa epoxide hydrolase, cystic fibrosis transmembr

126 tion and improves survival in response to P. aeruginosa ER-mediated processes may explain the sex-bas

127 y a previously unknown mechanism by which P. aeruginosa ExoY inhibits the host innate immune response

128 Thus, P. aeruginosa exploits the ParS sensing machinery to defend

129 Taken together, our findings suggest that P. aeruginosa exploits the precise spacing of collagen lame

130 After prolonged P. aeruginosa exposure, ASER-specific SOD-1 expression is d

131 ns of the opportunistic pathogen Pseudomonas aeruginosa express one of five different type IV pilins

132 P. aeruginosa formed antibiotic resistant biofilms on 3-D c

133 The opportunistic pathogen Pseudomonas aeruginosa forms antimicrobial resistant biofilms throug

134 approximately 50% of clinical isolates of P. aeruginosa from chronic airway infection in CF patients.

135 f PTEN, were unable to eradicate Pseudomonas aeruginosa from the airways and could not generate suffi

136 of Pf phage prevents the dissemination of P. aeruginosa from the lung.

137 Here, we demonstrate that the P. aeruginosa gene PA4463 [hibernation promoting factor (HP

138 P. aeruginosa GroEL, a homolog of heat shock protein 60, wa

139 and the active sites can abolish Pseudomonas aeruginosa growth in a defined medium with malonate as t

140 Mice infected with ExoY-deficient P. aeruginosa had higher levels of tumor necrosis factor (T

141 The efficiency of MBF-12 for M. aeruginosa harvesting could reach 95% under the optimiz

142 In vitro, C. albicans and P. aeruginosa have a bidirectional and largely antagonistic

143 h other pathogens, in particular Pseudomonas aeruginosa Here, we demonstrate that CF mice are highly

144 For Pseudomonas aeruginosa, human monoclonal antibodies (mAbs) targeting

145 totriose was also able to detect Pseudomonas aeruginosa in a clinically relevant mouse model of wound

146 ession of which impaired the virulence of P. aeruginosa in a murine model of systemic infection.

147 mportant clues regarding the virulence of P. aeruginosa in albumin-depleted versus albumin-rich infec

148 active biomarker for identifying Pseudomonas aeruginosa in clinical infections.

149 the detection of carbapenemase-producing P. aeruginosa, including all rapid chromogenic assays and t

150 thesis of LTB4 in the context of Pseudomonas aeruginosa-induced neutrophil transepithelial migration

151 fection of pulmonary endothelial cells by P. aeruginosa induces production and release of a cytotoxic

152 evels in CF epithelial cells and prevents P. aeruginosa infection in CF mice.

153 , and pyocyanin) and successfully inhibit P. aeruginosa infection in murine model of implant-associat

154 Pseudomonas aeruginosa infection liberates transmissible, cytotoxic

155 d its effects in a Caenorhabditis elegans-P. aeruginosa infection model.

156 rne stage in a murine bacteremic model of P. aeruginosa infection.

157 m pathogenic Candida albicans or Pseudomonas aeruginosa infection.

158 N, showed reduced plasma cytokines during P. aeruginosa infection.

159 improved the host response to a Pseudomonas aeruginosa infection.

160 during multidrug resistant (MDR)-Pseudomonas aeruginosa infections are limited.

161 Recurrent Pseudomonas aeruginosa infections coupled with robust, damaging neut

162 nd resistance during various types of MDR-P. aeruginosa infections is needed to define ceftolozane-ta

163 esistance in the severity and outcomes of P. aeruginosa infections is not yet well established.

164 elated factors influencing the outcome of P. aeruginosa infections, antibiotic resistance, and partic

165 sful in treating 71% of patients with MDR-P. aeruginosa infections, most of whom had pneumonia.

166 an important role in the pathogenicity of P. aeruginosa infections.

167 therapeutic alternative against pulmonary P. aeruginosa infections.

168 eated with ceftolozane-tazobactam for MDR-P. aeruginosa infections.

169 factors may also modulate the severity of P. aeruginosa infections.

170 Pseudomonas aeruginosa is a Gram-negative bacterial pathogen associa

171 Pseudomonas aeruginosa is a Gram-negative, opportunistic pathogen th

172 Pseudomonas aeruginosa is a major cause of severe infections that le

173 Pseudomonas aeruginosa is a pathogenic gram-negative organism that h

174 Pseudomonas aeruginosa is a significant contributor to recalcitrant

175 Pseudomonas aeruginosa is among the leading causes of severe nosocom

176 Pseudomonas aeruginosa is an important opportunistic human pathogen

177 Pseudomonas aeruginosa is an opportunistic and frequently drug-resis

178 The ubiquitous bacterium Pseudomonas aeruginosa is an opportunistic pathogen that can cause s

179 The pathogenic profile of P. aeruginosa is related to its ability to secrete a variet

180 we show that granule genesis in Pseudomonas aeruginosa is tightly organized under nitrogen starvatio

181 acterial pathogens, particularly Pseudomonas aeruginosa, is the primary cause of morbidity and mortal

182 ity against colistin-resistant strains of P. aeruginosa (isolated from cystic fibrosis patients) indi

183 tection of carbapenemase production among P. aeruginosa isolates and less reliable for use with A. ba

184 tal of 86% of the carbapenemase-producing P. aeruginosa isolates produced class B carbapenemases.

185 The consistent identification of both P. aeruginosa isolates was observed only in the presence of

186 tem effector found in 90% of the Pseudomonas aeruginosa isolates.

187 ae, Acinetobacter baumannii, and Pseudomonas aeruginosa isolates.

188 For Pseudomonas aeruginosa, it has long been known that intracellular le

189 an enhanced oxidative burst but decreased P. aeruginosa killing and earlier cell necrosis.

190 r biofilm-mediated resistance to Pseudomonas aeruginosa killing.

191 We find that P. aeruginosa LasA endopeptidase potentiates lysis of S. au

192 uence approximately 400 clinical Pseudomonas aeruginosa libraries and demonstrate excellent single-nu

193 Each P. aeruginosa LT was expressed as a soluble protein and eva

194 nfections by multidrug-resistant Pseudomonas aeruginosa (MDRPa) are an important cause of morbidity a

195 Here we defined PF orthologs in Pseudomonas aeruginosa, Moraxella catarrhalis, and Staphylococcus au

196 A Pseudomonas aeruginosa mutant lacking all three known iron acquisiti

197 Here we screen P. aeruginosa mutants defective in growth in iron-depleted

198 on the factors underlying the outcome of P. aeruginosa nosocomial infections, including aspects rela

199 Strikingly, WarA influences P. aeruginosa O antigen modal distribution and interacts wi

200 ch as invasive aspergillosis and Pseudomonas aeruginosa occurred during hospitalization.

201 The simulations reveal that although the P. aeruginosa OMs are thinner hydrophobic bilayers than the

202 Further, we observe the dimerization of P. aeruginosa outer domains without any perturbation of the

203 Pseudomonas aeruginosa (PA) is a ubiquitous microbe.

204 Here, we show that the bacterium Pseudomonas aeruginosa PA14 uses the cell-cell communication process

205 In the pathogenic bacterium Pseudomonas aeruginosa PA14, antibiotics called phenazines act as ox

206 on in the opportunistic pathogen Pseudomonas aeruginosa PA14.

207 CRISPR adaptive immune system in Pseudomonas aeruginosa (PA14) consists of two CRISPR loci and six CR

208 The responses of Pseudomonas aeruginosa PAO1 and PA14 to a hexadecane-water interface

209 d a single chemosensory pathway, Pseudomonas aeruginosa PAO1 has a much more complex chemosensory net

210 s close strain, the nonproducing Microcystis aeruginosa PCC 7005, grow similarly in the presence of 1

211 The microcystin-producing Microcystis aeruginosa PCC 7806 and its close strain, the nonproduci

212 fluid collected from human patients with P. aeruginosa pneumonia demonstrated cytotoxic activity, an

213 genetically sequenced strains (99.9%) of P. aeruginosa possess the two genes (PhzM and PhzS) necessa

214 largely contributes to heat tolerance of P. aeruginosa primarily in stationary phase and boosts heat

215 The opportunistic pathogen Pseudomonas aeruginosa produces the cationic exopolysaccharide Pel,

216 This cascade consists of four Pseudomonas aeruginosa protein regulators (ExsADCE) that sequester t

217 rs show that two DMAbs targeting Pseudomonas aeruginosa proteins confer protection against lethal pne

218 osphodiesterase domains from the Pseudomonas aeruginosa proteins PA3825 (PA3825(EAL)) and PA1727 (Muc

219 NB predicted to be specific for Pseudomonas aeruginosa (pyocin Sn) was produced and shown to kill P.

220 Analysis of a Pseudomonas aeruginosa quiC1 gene knock-out demonstrates that it is

221 uginosa and S. aureus We demonstrate that P. aeruginosa quorum sensing is inhibited by physiological

222 The P. aeruginosa quorum-sensing-deficient DeltalasR mutant als

223 While P. aeruginosa readily kills S. aureusin vitro, the two spec

224 us aureus, Escherichia coli, and Pseudomonas aeruginosa) relative to controls.

225 coli, Klebsiella pneumoniae, and Pseudomonas aeruginosa-reported here underscores the broad utility o

226 oreover, treatment of a lung infection of P. aeruginosa results in a large reduction in bacterial num

227 ed, infiltration of the corneal stroma by P. aeruginosa revealed a high degree of alignment between t

228 t HPF is the major factor associated with P. aeruginosa ribosome preservation.

229 ould provide important insights regarding P. aeruginosa's virulence mechanisms.

230 common pathogens in chronic wounds such as P.aeruginosa, S.aureus and Methicillin-resistant S.aureus

231 uorum sensing (QS) is a mechanism wherein P. aeruginosa secretes small diffusible molecules, specific

232 urs of incubation with nanoceria at pH 9, P. aeruginosa showed drastic morphological changes as a res

233 lude Acinetobacter baumannii and Pseudomonas aeruginosa (SNAP and POP studies).

234 gans first encounters pathogenic bacteria P. aeruginosa, SOD-1 is induced in the ASER neuron.

235 16 were nonhemolytic and retained potent P. aeruginosa-specific antimicrobial activity.

236 hia coli, Enterococcus faecalis, Pseudomonas aeruginosa, Staphylococcus aureus (including clinical is

237 aumannii, Klebsiella pneumoniae, Pseudomonas aeruginosa, Staphylococcus aureus, and coagulase-negativ

238 lso exhibited the highest efficiency when P. aeruginosa/Staphylococcus aureus co-culture RNA samples

239 umoniae, Legionella pneumophila, Pseudomonas aeruginosa, Stenotrophomonas maltophilia, Vibrio cholera

240 zation was facilitated through studying a P. aeruginosa strain lacking the RetS sensor, which has a f

241 abolic network reconstruction of Pseudomonas aeruginosa strain PA14 and an updated, expanded reconstr

242 ividual oxidants on the virulent Pseudomonas aeruginosa strain PA14.

243 nd an updated, expanded reconstruction of P. aeruginosa strain PAO1.

244 er, no subject eradicated their infecting P. aeruginosa strain, and after the first year P. aeruginos

245 strate that the pathogenicity of Pseudomonas aeruginosa strains derived from acute clinical infection

246 e inoculated with lux-engineered Pseudomonas aeruginosa strains isolated from equine uterine infectio

247 ructure-guided disulfide cross-linking in P. aeruginosa suggest that PelC assembles into a 12- subuni

248 ative DNA transfer in E. coli and trigger P. aeruginosa T6SS killing, but not pilus production.

249 tissue than mice infected with wild-type P. aeruginosa Taken together, our findings identify a previ

250 correlated with P. aeruginosa (E. coli vs P. aeruginosa tau = 0.090, p = 0.027; Enterococcus spp. vs

251 = 0.090, p = 0.027; Enterococcus spp. vs P. aeruginosa tau = 0.126, p = 0.002), but not the other OP

252 In other genomes such as Pseudomonas aeruginosa the bioH gene is within a biotin synthesis op

253 e most frequently colonized, and Pseudomonas aeruginosa the predominant organism.

254 pyocin Sn) was produced and shown to kill P. aeruginosa thereby validating our pipeline.

255 -regulating methyltransferase in Pseudomonas aeruginosa This cocrystal structure, together with the s

256 g increase in the sensitivity of Pseudomonas aeruginosa to ciprofloxacin.

257 to characterize the response of Pseudomonas aeruginosa to external 0.5 mm CuSO4, a condition that di

258 ng survival of other bacteria and helping P. aeruginosa to prevail in specific niches.

259 um signals, resulting in the inability of P. aeruginosa to produce virulence factors that kill S. aur

260 nce is key for maintaining the ability of P. aeruginosa to resuscitate from starvation-induced dorman

261 Here, we experimentally evolved Pseudomonas aeruginosa to six 2-drug sequences.

262 sensitivities of a ohr mutant of Pseudomonas aeruginosa toward different hydroperoxides.

263 The Pseudomonas aeruginosa type III secretion system delivers effector p

264 dispensable for activation of a Pseudomonas aeruginosa type VI secretion system (T6SS).

265 The adaptive immune system in Pseudomonas aeruginosa (type I-F) relies on a 350 kDa CRISPR RNA (cr

266 sentiality in the model organism Pseudomonas aeruginosa UCBPP-PA14.

267 eptide siderophore pyoverdine by Pseudomonas aeruginosa, under different nutrient-limiting conditions

268 veloped either an E. faecalis or Pseudomonas aeruginosa urinary tract infection, suggesting a role fo

269 harvest the typical microalgae, Microcystis aeruginosa, using a bioflocculant produced by Citrobacte

270 clude that three chemosensory pathways in P. aeruginosa utilize one chemoreceptor per pathway, wherea

271 portunistic pathogenic bacterium Pseudomonas aeruginosa via an unknown pathway.

272 We hypothesize that hypoxia reduces P. aeruginosa virulence at least in part through the regula

273 ential strategy not only for induction of P. aeruginosa virulence but also for maintaining viability

274 The likely more deeply studied P. aeruginosa virulence determinant is the type III secreti

275 olone signal (PQS) compound is a secreted P. aeruginosa virulence factor that contributes to the path

276 P. aeruginosa virulence is controlled partly by intercellul

277 s an effective strategy for abrogation of P. aeruginosa virulence.

278 Microcystis aeruginosa was cultured in the medium containing low and

279 When P. aeruginosa was isolated, the TTD was typically <26 h, an

280 n vivo Pf phage production was inhibited, P. aeruginosa was less virulent.

281 thelial barrier function against Pseudomonas aeruginosa was MyD88-dependent.

282 cal variables, and it was determined that P. aeruginosa was the only OPPP positively associated with

283 uropathogens (Escherichia coli, Pseudomonas aeruginosa) was also explored, and thioridazine was show

284 h that of its ortholog LecA from Pseudomonas aeruginosa We also investigated the utility of PllA as a

285 man subjects were tested for responses to P. aeruginosa We found that female mice inoculated with P.

286 alis, Klebsiella pneumoniae, and Pseudomonas aeruginosa We therefore conclude that the underlying mec

287 sex hormones on host immune responses to P. aeruginosa We used wild-type and CF mice, which we hormo

288 that contributes to the pathogenicity of P. aeruginosa We were able to detect PQS in sputum samples

289 ress the need for new agents to treat MDR P. aeruginosa, we focused on inhibiting the first committed

290 assumption that temocillin is inactive on P. aeruginosa, we show here clinically-exploitable MICs on

291 aboratory strains of Escherichia coli and P. aeruginosa were killed by a process of condensing intrac

292 te secreted by a toxic strain of Microcystis aeruginosa were studied by measuring reactive oxygen spe

293 mal inhibitory concentration for Pseudomonas aeruginosa) were compared between the two groups.

294 s (Sph3h from A. fumigatus and PelAh from P. aeruginosa) were found to degrade their respective polys

295 ations did cause a delay in the growth of P. aeruginosa, whereas impressively S. epidermidis did not

296 resistant Enterobacteriaceae and Pseudomonas aeruginosa, which are difficult to treat.

297 fected with carbapenem-resistant Pseudomonas aeruginosa who were treated with ceftolozane/tazobactam

298 xic strain of the cyanobacterium Microcystis aeruginosa with Fe(II) and Fe(III) was investigated here

299 utive epithelial barrier function against P. aeruginosa, with details dependent upon in vivo conditio

300 cultures, suggesting that Pf phage traps P. aeruginosa within the lung.