ライフサイエンスコーパス: P. aeruginosa

1 P. aeruginosa adhered avidly to lung vasculature, where

2 P. aeruginosa defective in the stringent response also h

3 P. aeruginosa expresses a type III secretion system (T3S

4 P. aeruginosa formed antibiotic resistant biofilms on 3-

5 P. aeruginosa gene expression patterns from sputum clust

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

7 P. aeruginosa has evolved numerous evasion and subversio

8 P. aeruginosa isolates from CF patients failed to induce

9 P. aeruginosa transcript profiles in RNA from CF sputum

10 P. aeruginosa virulence is controlled partly by intercel

11 hours of incubation with nanoceria at pH 9, P. aeruginosa showed drastic morphological changes as a

12 erization was facilitated through studying a P. aeruginosa strain lacking the RetS sensor, which has

13 domonas aeruginosa and subsequently abundant P. aeruginosa clone C.

14 We identified 114 patients with acute P. aeruginosa BSI; 56 cases were accompanied by acute se

15 chia coli (E. coli), Pseudomonas aeruginosa (P. aeruginosa), Staphylococcus aureus (S. aureus) and St

16 cus aureus, MRSA and Pseudomonas aeruginosa, P. aeruginosa) were analyzed in bronchoalveolar lavage (

17 Single-dose phage therapy was active against P. aeruginosa EE and highly synergistic with ciprofloxac

18 showed stronger inhibitory activity against P. aeruginosa associated with plastic compared to 3-D ce

19 However, anti-Psl mAb activity against P. aeruginosa biofilms is unknown.

20 rophylactic and therapeutic activity against P. aeruginosa during gut infection in two animal models

21 directly contribute to its activity against P. aeruginosa.

22 the efficacy of most antimicrobials against P. aeruginosa biofilm formation, which in turn depends o

23 l role for PPARgamma in host defense against P. aeruginosa Strategies that activate PPARgamma can pro

24 titutive epithelial barrier function against P. aeruginosa, with details dependent upon in vivo condi

25 splayed acceptable bacterial killing against P. aeruginosa ATCC 27853 and no nephrotoxicity was found

26 these observations suggest that C. albicans-P. aeruginosa cross talk in vivo can benefit both organi

27 ant virulence factors produced by nearly all P. aeruginosa strains, and other species do not produce

28 surface signaling system through HasA allows P. aeruginosa to rapidly respond to fluctuating extracel

29 detection of carbapenemase production among P. aeruginosa and A. baumannii Ten testing sites then ev

30 detection of carbapenemase production among P. aeruginosa isolates and less reliable for use with A.

31 highest in Acinetobacter species (71.9%) and P. aeruginosa (23.6%).

32 lung infection and show that C. albicans and P. aeruginosa are synergistically virulent.

33 In vitro, C. albicans and P. aeruginosa have a bidirectional and largely antagonis

34 development for C. difficile, S. aureus, and P. aeruginosa Basic, preclinical, and early clinical res

35 exchange mechanism for both the E. coli and P. aeruginosa systems, identifying helix 13 of EF-Ts as

36 Laboratory strains of Escherichia coli and P. aeruginosa were killed by a process of condensing int

37 We conclude that hyperglycaemia and P. aeruginosa induce a metabolic shift which increases l

38 evidence for association of F. nucleatum and P. aeruginosa with OSCC.

39 03) and decreased for Acinetobacter spp. and P. aeruginosa (P < 0.0001).

40 lize Ent, including some E. coli strains and P. aeruginosa.

41 capable of producing a biofilm in vitro, and P. aeruginosa is capable of producing biofilm-like mater

42 pathogens that cause the corneal ulcers are P. aeruginosa and S. aureus.

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

44 the biofilm and promotes interaction between P. aeruginosa and Staphylococcus aureus.

45 environment to modulate interactions between P. aeruginosa and S. aureus We demonstrate that P. aerug

46 dly versus antagonistic interactions between P. aeruginosa and S. aureus.

47 During growth in a biofilm, P. aeruginosa dramatically increases the production of f

48 ts between CFU and relative bioluminescence; P. aeruginosa ATCC9027 tatH5-pMElux is the best construc

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

50 asis for mucin-based nutrient acquisition by P. aeruginosa and reveal a host-pathogen dynamic that ma

51 a novel mechanism of pathogen adaptation by P. aeruginosa to avoid detection by inflammasomes in CF

52 infection of pulmonary endothelial cells by P. aeruginosa induces production and release of a cytoto

53 rH, are required for acute lung infection by P. aeruginosa Moreover, we show that the virulence defec

54 also demonstrate that oxylipins produced by P. aeruginosa promote virulence in Drosophila flies and

55 ly acyl-homoserine lactones, are produced by P. aeruginosa to promote virulence.

56 ested, infiltration of the corneal stroma by P. aeruginosa revealed a high degree of alignment betwee

57 are among the key virulence factors used by P. aeruginosa for host cell attachment, biofilm formatio

58 hese 75 transcripts are stable in chronic CF P. aeruginosa lung infections.

59 nosa virulence or that can eradicate chronic P. aeruginosa lung infections associated with cystic fib

60 atory response in a murine pulmonary chronic P. aeruginosa model.

61 voltammetric scans of 94 different clinical P. aeruginosa isolates were taken to measure the concent

62 as a new innate defense mechanism to control P. aeruginosa infection, but at the same time potentiall

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

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

65 tive use with antibiotics to inhibit/disrupt P. aeruginosa biofilms as a result of chronic infection.

66 h3h In contrast, Sph3h was unable to disrupt P. aeruginosa Pel-based biofilms, despite being able to

67 planation for the ability of EGCG to disrupt P. aeruginosa QS and modify its biofilm and strengthens

68 ermore, D-RR4 was more capable of disrupting P. aeruginosa and A. baumannii biofilms when compared to

69 Treatment with PodA disrupts P. aeruginosa biofilm formation similarly to DNase, sugg

70 F lung appears to play a key role in driving P. aeruginosa diversification.

71 -ODN, showed reduced plasma cytokines during P. aeruginosa infection.

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

73 ored its effects in a Caenorhabditis elegans-P. aeruginosa infection model.

74 anding" E. coli BioH with the operon-encoded P. aeruginosa BioH.

75 that improved CFTR trafficking could enhance P. aeruginosa clearance from the CF airway by activating

76 that improved CFTR trafficking could enhance P. aeruginosa clearance through activating the tumor sup

77 e cells (E. coli, B. subtilis, Enterococcus, P. aeruginosa and Salmonella typhi) to antibiotics such

78 tilizing bioluminescence imaging with equine P. aeruginosa isolates from this study.

79 be facilitated by an approach that explores P. aeruginosa gene function in systems-level models.

80 S2(NTD) being imported into FpvAI-expressing P. aeruginosa cells by a process analogous to that used

81 5% 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.

82 5 antimicrobials were evaluated, with 11 for P. aeruginosa, 14 for A. baumannii, and 2 for S. maltoph

83 use of antibiotics are key risk factors for P. aeruginosa infections, whereas underlying disease, so

84 ggest a role for PPARgamma immunotherapy for P. aeruginosa infections.

85 n CFU, and minimal effects were observed for P. aeruginosa isolates.

86 o identify genetic determinants required for P. aeruginosa growth using intact purified mucins as a s

87 The CA values for P. aeruginosa, A. baumannii, and S. maltophilia were 94.

88 The essential agreement values for P. aeruginosa, A. baumannii, and S. maltophilia were 99.

89 well as RNA serial sputum samples from four P. aeruginosa-colonized subjects with CF collected over

90 Conditioned media from P. aeruginosa infected epithelial cells induced a potent

91 very low doses, they protected the mice from P. aeruginosa infection-related changes in lung histolog

92 eins (Sph3h from A. fumigatus and PelAh from P. aeruginosa) were found to degrade their respective po

93 hemical detection of pyocyanin secreted from P. aeruginosa strains while optically imaging the cells.

94 lavage of lung transplant recipients growing P. aeruginosa (11.5 [5.4-21.8] vs. 2.8 [0.9-9.4] pg/mL,

95 rown cultures; in contrast, laboratory-grown P. aeruginosa showed much greater transcriptional variat

96 nging survival of other bacteria and helping P. aeruginosa to prevail in specific niches.

97 Overall, this work sheds light on how P. aeruginosa triggers a pro-inflammatory response and c

98 However, P. aeruginosa airway infection persisted.

99 f this approach by isolating and identifying P. aeruginosa and P. fluorescens from tap water samples,

100 iderophore receptors for iron acquisition in P. aeruginosa.

101 otential persistence and virulence factor in P. aeruginosa.

102 Functional amyloid fibrils in P. aeruginosa (Fap) are able to bind and retain quorum-s

103 P. aeruginosa Here, we show that QS genes in P. aeruginosa (strain PAO1) and 3O-C12-HSL attenuate PPA

104 R levels were 73-fold and 210-fold higher in P. aeruginosa and Acinetobacter spp., respectively.

105 cyl carrier protein AcpP, were identified in P. aeruginosa.

106 ransporters that control the Cu(+) levels in P. aeruginosa compartments.

107 structure-guided disulfide cross-linking in P. aeruginosa suggest that PelC assembles into a 12- sub

108 omponents of the type IVa pilus machinery in P. aeruginosa, with PilM binding to PilB, PilT, and PilC

109 motive force of the cytoplasmic membrane in P. aeruginosa.

110 significantly increased swarming motility in P. aeruginosa.

111 of the first known roles of the PTS(Ntr) in P. aeruginosa.

112 conclude that three chemosensory pathways in P. aeruginosa utilize one chemoreceptor per pathway, whe

113 imited information about the role of PhoQ in P. aeruginosa bloodstream infections.

114 of iron utilization plays a critical role in P. aeruginosa's ability to survive during infection.

115 red expression of the sRNAs RsmY and RsmZ in P. aeruginosa and the small dual-function regulatory RNA

116 -specific fluorescent thioflavin T signal in P. aeruginosa biofilms at concentrations known to exert

117 nhibition of small regulatory RNAs (sRNA) in P. aeruginosa as well as in Staphylococcus aureus, anoth

118 overed a novel, targetable defense system in P. aeruginosa.

119 lagellar filaments in B. subtilis and two in P. aeruginosa capture two different states of the filame

120 hus, we evaluated inhibition of virulence in P. aeruginosa by a designed peptide (RpoN molecular road

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

122 ns produced within a population of infecting P. aeruginosa may have selected for bacterial mutants th

123 wever, no subject eradicated their infecting P. aeruginosa strain, and after the first year P. aerugi

124 st within the host during chronic infection, P. aeruginosa must evade inflammasome activation, and pu

125 During infection, P. aeruginosa enters the terminal bronchioles and alveol

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

127 pid, and pyocyanin) and successfully inhibit P. aeruginosa infection in murine model of implant-assoc

128 K-5 exhibited more potent ability to inhibit P. aeruginosa association with both substrates.

129 The ability of raffinose to inhibit P. aeruginosa biofilm formation and its molecular mechan

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

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

132 and subversion mechanisms in tandem to kill P. aeruginosa.

133 articles were much more effective at killing P. aeruginosa and S. epidermidis at basic pH values (pH

134 inal concentrations of 0.01 mg/L and 1 mg/L, P. aeruginosa adsorbed considerable amounts of MWCNTs: (

135 onella larvae from the lethal effects of MDR P. aeruginosa.

136 address the need for new agents to treat MDR P. aeruginosa, we focused on inhibiting the first commit

137 ybrid possesses potent activity against MDR, P. aeruginosa isolates the activity that can be synergiz

138 treated with ceftolozane-tazobactam for MDR-P. aeruginosa infections.

139 s and resistance during various types of MDR-P. aeruginosa infections is needed to define ceftolozane

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

141 used dual RNA-seq to simultaneously measure P. aeruginosa and the murine host's gene expression and

142 ly, in both the in vitro and in vivo models, P. aeruginosa did not appear to cross the corneal limbus

143 activity in a large collection (n = 333) of P. aeruginosa CF isolates.

144 649 genetically sequenced strains (99.9%) of P. aeruginosa possess the two genes (PhzM and PhzS) nece

145 n model, we implicate WarA in the ability of P. aeruginosa to evade detection by the host.

146 in microcolonies, increasing the ability of P. aeruginosa to form biofilms in vitro and in vivo (in

147 enance is key for maintaining the ability of P. aeruginosa to resuscitate from starvation-induced dor

148 s is an effective strategy for abrogation of P. aeruginosa virulence.

149 technology to monitor relative abundances of P. aeruginosa transcripts across clinical isolates, in s

150 n is a previously unrecognized adaptation of P. aeruginosa to the lung of individuals with CF that fa

151 Through our analyses of P. aeruginosa and six Streptococci, we show that ensembl

152 lence and the ability to cause bacteremia of P. aeruginosa.

153 preformed biofilms or decreasing the CFU of P. aeruginosa and K. pneumoniae within a biofilm.

154 PPARgamma agonists also enhance clearance of P. aeruginosa from lungs of mice infected with PAO1.

155 ciated with its detection, in the context of P. aeruginosa gene expression and multicellular behavior

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

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

158 ts of Pf phage prevents the dissemination of P. aeruginosa from the lung.

159 Importantly, exposure of P. aeruginosa to CF-ALF drives the activation of neutrop

160 sustained inhibitory effect on the growth of P. aeruginosa and can reduce the number of viable coloni

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

162 ntrations did cause a delay in the growth of P. aeruginosa, whereas impressively S. epidermidis did n

163 further demonstrated for in vivo imaging of P. aeruginosa in implant and corneal infection mice mode

164 uorum signals, resulting in the inability of P. aeruginosa to produce virulence factors that kill S.

165 essential strategy not only for induction of P. aeruginosa virulence but also for maintaining viabili

166 Moreover, treatment of a lung infection of P. aeruginosa results in a large reduction in bacterial

167 orhabditis elegans from lethal infections of P. aeruginosa and A. baumannii and enhanced the activity

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

169 rientation of an invasive corneal isolate of P. aeruginosa in the corneal stroma during infection of

170 nd approximately 50% of clinical isolates of P. aeruginosa from chronic airway infection in CF patien

171 reased activity against clinical isolates of P. aeruginosa, further confirming the target pathway.

172 A vast majority of P. aeruginosa BSI isolates express PcrV and Psl; however

173 monolayers) that mimic the inner membrane of P. aeruginosa The study demonstrated the interaction of

174 -borne stage in a murine bacteremic model of P. aeruginosa infection.

175 s, show strong efficacy in a murine model of P. aeruginosa lung infection, with the concentration of

176 the current hierarchical regulation model of P. aeruginosa QS systems by revealing new interconnectio

177 ype IV pilus-dependent twitching motility of P. aeruginosa.

178 ations because of the frequent occurrence of P. aeruginosa and S. aureus co-infections.

179 cule that promotes the opsonophagocytosis of P. aeruginosa.

180 n-related factors influencing the outcome of P. aeruginosa infections, antibiotic resistance, and par

181 dge on the factors underlying the outcome of P. aeruginosa nosocomial infections, including aspects r

182 c resistance in the severity and outcomes of P. aeruginosa infections is not yet well established.

183 In this study, we utilize a panel of P. aeruginosa burn wound and cystic fibrosis (CF) lung i

184 contribution of hepP to the pathogenesis of P. aeruginosa during burn wound infection.

185 ay an important role in the pathogenicity of P. aeruginosa infections.

186 tor that contributes to the pathogenicity of P. aeruginosa We were able to detect PQS in sputum sampl

187 e and pH were exacerbated by the presence of P. aeruginosa and were attenuated by inhibition of monoc

188 hat in in vitro experiments, pretreatment of P. aeruginosa with rMIF is associated with reduced bacte

189 The pathogenic profile of P. aeruginosa is related to its ability to secrete a var

190 ement and enhanced neutrophil recognition of P. aeruginosa, neutrophil-mediated clearance of the path

191 4 and an updated, expanded reconstruction of P. aeruginosa strain PAO1.

192 s spectrometric analysis of the secretome of P. aeruginosa derived from an acute infection revealed h

193 ic factors may also modulate the severity of P. aeruginosa infections.

194 tivity against colistin-resistant strains of P. aeruginosa (isolated from cystic fibrosis patients) i

195 cyanin by all clinically-relevant strains of P. aeruginosa is a significant step towards validating t

196 emergence of antibiotic-resistant strains of P. aeruginosa, there is an urgent need to develop novel

197 production occurs in all clinical strains of P. aeruginosa.

198 n Pseudomonas aeruginosa Previous studies of P. aeruginosa virulence, physiology, and biofilm develop

199 lpG largely contributes to heat tolerance of P. aeruginosa primarily in stationary phase and boosts h

200 be advanced by an improved understanding of P. aeruginosa behavior in vivo We demonstrate the use of

201 further pathophysiological understanding of P. aeruginosa biofilms.

202 h Psl and PcrV enhanced neutrophil uptake of P. aeruginosa and also greatly increased inhibition of T

203 CF lung disease was measured in a variety of P. aeruginosa strains as well as RNA serial sputum sampl

204 xpression of which impaired the virulence of P. aeruginosa in a murine model of systemic infection.

205 e important clues regarding the virulence of P. aeruginosa in albumin-depleted versus albumin-rich in

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

207 Additionally, when producing Pf phage, P. aeruginosa was less prone to phagocytosis by macropha

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

209 e levels in CF epithelial cells and prevents P. aeruginosa infection in CF mice.

210 -culture with a competing PVDPAO1 -producer, P. aeruginosa PAO1.

211 f >90% for detecting carbapenemase-producing P. aeruginosa Class D carbapenemases were the most preva

212 total of 86% of the carbapenemase-producing P. aeruginosa isolates produced class B carbapenemases.

213 ficity for detecting carbapenemase-producing P. aeruginosa isolates.

214 for the detection of carbapenemase-producing P. aeruginosa, including all rapid chromogenic assays an

215 entiated by the presence of a LasA-producing P. aeruginosa population.

216 After prolonged P. aeruginosa exposure, ASER-specific SOD-1 expression i

217 ere, we show that both modifications protect P. aeruginosa from certain pilus-specific phages.

218 us therapeutic alternative against pulmonary P. aeruginosa infections.

219 We hypothesize that hypoxia reduces P. aeruginosa virulence at least in part through the reg

220 t could provide important insights regarding P. aeruginosa's virulence mechanisms.

221 echanistic insights into how Chil1 regulates P. aeruginosa-induced host responses.

222 colistin in vivo against colistin-resistant P. aeruginosa.

223 peutic complement for treatment of resistant P. aeruginosa infections.

224 Here we screen P. aeruginosa mutants defective in growth in iron-deplet

225 tiviral interferons promote robust secondary P. aeruginosa biofilm formation.

226 Here, we show that a secreted P. aeruginosa epoxide hydrolase, cystic fibrosis transme

227 uinolone signal (PQS) compound is a secreted P. aeruginosa virulence factor that contributes to the p

228 ia mellonella infection model and sensitizes P. aeruginosa to serum complement activity.

229 Ivacaftor caused marked reductions in sputum P. aeruginosa density and airway inflammation and produc

230 ichia coli in Conjunctivitis; Staphylococci, P. aeruginosa and E. coli in dacryocystitis; Coagulase n

231 The likely more deeply studied P. aeruginosa virulence determinant is the type III secr

232 ich distinguishes it from other well-studied P. aeruginosa phenazines.

233 interior of the filament among B. subtilis, P. aeruginosa and Salmonella enterica.

234 were isolated 11 times more frequently than P. aeruginosa and Acinetobacter spp.

235 concentrations also decreased, but less than P. aeruginosa.

236 rosis (CF) lung isolates to demonstrate that P. aeruginosa alters S. aureus susceptibility to bacteri

237 Together, these data demonstrate that P. aeruginosa impairs the ability of host cells to mount

238 aeruginosa and S. aureus We demonstrate that P. aeruginosa quorum sensing is inhibited by physiologic

239 ogical variables, and it was determined that P. aeruginosa was the only OPPP positively associated wi

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

241 However, given that P. aeruginosa, particularly in its biofilm mode of growt

242 ation and chemical inhibition, indicate that P. aeruginosa contains multiple enzymes that catalyze th

243 These findings indicate that P. aeruginosa produces a biofilm in the uterus and that

244 flammasomes in CF patients and indicate that P. aeruginosa-activated inflammasomes are not involved i

245 network based on PseudomonasNet reveals that P. aeruginosa has common modular genetic organisations t

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

247 The P. aeruginosa quorum-sensing-deficient DeltalasR mutant

248 expression of additional 35 loci across the P. aeruginosa genome, including major regulators and vir

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

250 We recently described the P. aeruginosa heparinase-encoding gene, hepP, whose expr

251 factor PqsR is a necessary component in the P. aeruginosa cell-to-cell signaling network.

252 CF-ALF influences the P. aeruginosa cell wall by reducing the content of one o

253 osion current density in the presence of the P. aeruginosa biofilm in the 2216E medium.

254 PcrV is an essential part of the P. aeruginosa type III secretion system (T3SS), and its

255 Here, we demonstrate that the P. aeruginosa gene PA4463 [hibernation promoting factor

256 Thirty P. aeruginosa and 30 A. baumannii isolates previously ch

257 Thus, P. aeruginosa exploits the ParS sensing machinery to def

258 Administration of the flavonoids to P. aeruginosa alters transcription of quorum sensing-con

259 se, we profiled the acute immune response to P. aeruginosa and identified the pro-inflammatory cytoki

260 unction and improves survival in response to P. aeruginosa ER-mediated processes may explain the sex-

261 roposed as important in the host response to P. aeruginosa infection through their role in augmenting

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

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

264 strated that Chil1-deficient mice succumb to P. aeruginosa infection more rapidly than the wild type

265 plemented with 17beta-estradiol succumbed to P. aeruginosa challenge earlier than progesterone- or ve

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

267 fluorescence bio-barcode technology to trace P. aeruginosa ETA.

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

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

270 eradication concentration against wild-type P. aeruginosa biofilms, whereas EGCG had a more pronounc

271 ung tissue than mice infected with wild-type P. aeruginosa Taken together, our findings identify a pr

272 h flow (Pe > 102) suppressed QS in wild-type P. aeruginosa.

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

274 a pivotal role in host response to virulent P. aeruginosa Here, we show that QS genes in P. aerugino

275 he same regulations were observed in in vivo P. aeruginosa proliferation.

276 In vivo, P. aeruginosa traveled throughout the stroma in discrete

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

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

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

280 t also exhibited the highest efficiency when P. aeruginosa/Staphylococcus aureus co-culture RNA sampl

281 e expression was significantly enhanced when P. aeruginosa strain UCBPP_PA14 (PA14) was grown in whol

282 m medium, mimicking sputum of CF lungs where P. aeruginosa is an important pathogen and undergoes evo

283 Quorum sensing (QS) is a mechanism wherein P. aeruginosa secretes small diffusible molecules, speci

284 tify a previously unknown mechanism by which P. aeruginosa ExoY inhibits the host innate immune respo

285 While P. aeruginosa readily kills S. aureusin vitro, the two s

286 that HPF is the major factor associated with P. aeruginosa ribosome preservation.

287 B were positively but weakly correlated with P. aeruginosa (E. coli vs P. aeruginosa tau = 0.090, p =

288 ivo, New Zealand white rabbits were fit with P. aeruginosa laden contact lenses in the absence of a p

289 proved survival in female mice infected with P. aeruginosa and restored neutrophil function.

290 putum samples from CF patients infected with P. aeruginosa but not in samples from uninfected patient

291 ) and wild-type mice (WT mice) infected with P. aeruginosa had robust IL-17 production early in the i

292 sa We found that female mice inoculated with P. aeruginosa died earlier and showed slower bacterial c

293 hich we hormone manipulated, inoculated with P. aeruginosa, and then examined for outcomes and inflam

294 The co-complex structure of N42FTA with P. aeruginosa FabA protein rationalises affinity and sug

295 mals which was similar to that observed with P. aeruginosa infection.

296 age fluid collected from human patients with P. aeruginosa pneumonia demonstrated cytotoxic activity,

297 n about the interaction of this protein with P. aeruginosa isolates from individuals with cystic fibr

298 Furthermore, C5a synergises with P. aeruginosa LPS in both PD-L1 expression and the produ

299 tokine production were lower than those with P. aeruginosa The ability of host immune cells to recogn

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