ライフサイエンスコーパス: P. aeruginosa

1 P. aeruginosa adhesion to host epithelial cells is enhan

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

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

4 P. aeruginosa evades antibiotics in bacterial biofilms b

5 P. aeruginosa harbours hundreds of regulatory genes that

6 P. aeruginosa has multiple sigma factors to regulate tra

7 P. aeruginosa lung infections are difficult to treat bec

8 P. aeruginosa produces lectins LecA and LecB, which poss

9 P. aeruginosa Type I-C Cascade-Cas3 (PaeCas3c) facilitat

10 P. aeruginosa was isolated from 90 examined fish (31.57%

11 P. aeruginosa was most significantly associated with dev

12 P. aeruginosa, B. subtilis and S. aureus were used as a

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

14 y, we used a heterogeneous collection of 197 P. aeruginosa that included multidrug-resistant isolates

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

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

17 ty, biofilm formation, and pathogenesis in a P. aeruginosa-C. elegans infection model.

18 th analysis of the QS-mediated response of a P. aeruginosa antibiotic resistant mutant that overexpre

19 cificity was highlighted in the context of a P. aeruginosa biofilm, in which phanorod irradiation kil

20 o increase flap survival in the context of a P. aeruginosa infection associated with a foreign body.

21 resistance in P. aeruginosa We found that a P. aeruginosa strain lacking PPHD (PAO310) exhibits incr

22 ll as resistance to other antibiotics-across P. aeruginosa isolated from different patients.

23 The characterization of ErfA regulon across P. aeruginosa subfamilies revealed a second conserved ta

24 he production and secretion of redox-active, P. aeruginosa-produced phenazines, which reduce Fe(III)

25 ctions by pathogenic Pseudomonas aeruginosa (P. aeruginosa) remain to be properly addressed.

26 ence, antibiogram of Pseudomonas aeruginosa (P. aeruginosa), and the distribution of virulence genes

27 examine how loss of GSH biosynthesis affects P. aeruginosa virulence.

28 olerance regulatory circuits of SagS affects P. aeruginosa pathogenicity in chronic but not acute inf

29 best compound 26, displayed activity against P. aeruginosa and S. pseudintermedius, but not the close

30 novel role in pulmonary host defense against P. aeruginosa infection by facilitating crosstalk betwee

31 nt bacteria inhabitation and killing against P. aeruginosa infection, through lectin blocking and the

32 osine receptor signaling and protect against P. aeruginosa-induced acute lung injury.

33 rated that ENT1/2 blockade protected against P. aeruginosa -induced acute lung injury via activation

34 or fosfomycin susceptibility testing against P. aeruginosa and stress the need for P. aeruginosa-spec

35 data suggest that feedback inhibition allows P. aeruginosa to direct its effector arsenal against the

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

37 coagulase-negative staphylococci (21%), and P. aeruginosa (16%), 394 (24%) received IEAT despite IDS

38 for Enterobacteriaceae (76.4 vs. 32.9%) and P. aeruginosa (25.6 vs. 0.3%).

39 259 days and 147 days against S. aureus and P. aeruginosa, respectively, compared to 70 days of acti

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

41 h CF clinical isolates of B. cenocepacia and P. aeruginosa.

42 ureus and 16- to 64-fold against E. coli and P. aeruginosa alongside reduced cytotoxicity.

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

44 apenemase families from Enterobacterales and P. aeruginosa colonies on commonly used agar media.

45 rs with 110 isolates of Enterobacterales and P. aeruginosa These results were compared to the expecte

46 was 94.8% and 95.8% for Enterobacterales and P. aeruginosa, respectively (no breakpoints are currentl

47 for colistin testing of Enterobacterales and P. aeruginosa.

48 ginosa, and Enterobacter species(ESKAPE) and P. aeruginosa pathogens.

49 -target bacteria S. aureus, K. pneumonia and P. aeruginosa.

50 fection with A. baumannii, K. pneumoniae and P. aeruginosa.

51 MICs) against canine S. pseudintermedius and P. aeruginosa isolates as well rapid killing kinetics.

52 and Staphylococcus aureus with antagonistic P. aeruginosa.

53 ings suggest certain mutations that arise as P. aeruginosa adapts to the CF lung abrogate T6SS activi

54 Isolates from each medium identified as P. aeruginosa or Enterobacteriaceae were tested for susc

55 terize Scnn1b-transgenic (Tg) BALB/c mice as P. aeruginosa lung infection models.

56 ocytosed inhaled bacterial pathogens such as P. aeruginosa and S. aureus, cloaking the bacteria from

57 Airway infection with Proteobacteria such as P. aeruginosa was associated with higher concentrations

58 denosine levels and significantly attenuated P. aeruginosa-induced acute lung injury, as assessed by

59 Upon sensing S. aureus, P. aeruginosa transitioned from collective to single-cel

60 Methicillin-resistant S. aureus, P. aeruginosa, C. difficile, and fungal infections all h

61 wder exhibit >=99.9% reduction in S. aureus, P. aeruginosa, K. aerogenes and E.

62 ng infections are difficult to treat because P. aeruginosa adapts to the CF lung, can develop multidr

63 1 to 7) showed no activity and did not bind P. aeruginosa pili; nor did recombinant DMBT1 (aa 1-220)

64 Both P. aeruginosa and Bcc use type VI secretion systems (T6S

65 Both P. aeruginosa and S. aureus require iron to infect the m

66 Since both P. aeruginosa DsbB1 and M. tuberculosis VKOR complement

67 f BfmRS may contribute to host adaptation by P. aeruginosa during chronic infections.

68 isms, only patients with infection caused by P. aeruginosa experienced a significant increase in mort

69 r the infection of Caenorhabditis elegans by P. aeruginosa, the precise pathways and mechanism(s) of

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

71 inhibition of insects and mammalian hosts by P. aeruginosa utilizes the well-known exotoxin A effecto

72 prevents T6SS-dependent bacterial killing by P. aeruginosa.

73 e conclude that active cellular processes by P. aeruginosa afford a significant benefit to S. maltoph

74 outer membrane perturbation can be sensed by P. aeruginosa to activate the T6SS even when the disrupt

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

76 he in vitro biofilm evolution of an early CF P. aeruginosa isolate, AA2, in the presence or absence o

77 Challenging P. aeruginosa cells with the 4-substituted isoindoline a

78 lms by S. aureus and laboratory and clinical P. aeruginosa isolates.

79 the most common effectors found in clinical P. aeruginosa isolates.

80 mCIM) against a large collection of clinical P. aeruginosa isolates (n = 103) to provide clinicians a

81 ng activity against a collection of clinical P. aeruginosa isolates and is active in a Galleria mello

82 43 compromises clearance of wound-colonizing P. aeruginosa bacteria and exacerbates infection-induced

83 We used a diverse set of 58 complete P. aeruginosa genomes to curate a set of 4,440 core gene

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

85 that phagocytes are crucial for controlling P. aeruginosa infections, our data suggest that feedback

86 may inspire novel approaches for controlling P. aeruginosa infections.

87 Furthermore, PPHD-deficient P. aeruginosa displayed enhanced antibiotic resistance a

88 that the raGNPs/NS-MFS can successful detect P. aeruginosa and S. aureus in human plasma, and is very

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

90 c WT mice with FABP4(-/-) bone marrow during P. aeruginosa pneumonia, thus confirming the role of mac

91 Although early P. aeruginosa CF infection is thought to reflect acquisi

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

93 experimental biofilm environment, the early P. aeruginosa CF isolate AA2 evolves towards a CF-like g

94 nicity of hundreds of genetically engineered P. aeruginosa mutants is needed.

95 susceptibility testing of Enterobacterales, P. aeruginosa, and A. baumannii complex isolates with li

96 , 93.3%, and 89.2% for the Enterobacterales, P. aeruginosa, and the A. baumannii complex, respectivel

97 biology assays, we demonstrate that exposing P. aeruginosa and S. aureus cells to sphingosine results

98 Two extracellular P. aeruginosa lectins, LecA and LecB, are essential stru

99 he anti-staphylococcal compound facilitating P. aeruginosa dominance under normoxia and anoxia is gre

100 .62 and 5.27 +/- 1.10 vs. 4.74 +/- 1.06) for P. aeruginosa and OPP-C, respectively.

101 .44 and 3.87 +/- 0.78 vs. 3.21 +/- 1.11) for P. aeruginosa and OPP-C, respectively.

102 EA was 98.3% for P. aeruginosa and 91.6% for the A. baumannii complex whe

103 ng, thereby providing a growth advantage for P. aeruginosa in bacterial competition.

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

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

106 gainst P. aeruginosa and stress the need for P. aeruginosa-specific breakpoints.

107 previously between purified components from P. aeruginosa and could help channeling the NO (directly

108 vidence of de-N-acetylated muropeptides from P. aeruginosa The method developed here offers a robust

109 utase/phosphoglucomutase (alphaPMM/PGM) from P. aeruginosa is involved in bacterial cell wall assembl

110 ZapA from other bacterial species, ZapA from P. aeruginosa induced PaFtsZ protofilaments to associate

111 Fourteen patients (50%) had P. aeruginosa isolates which developed high-level TOL-TA

112 The 28 patients had P. aeruginosa isolates available both before and after T

113 Hence P. aeruginosa is able to differentiate c-di-GMP output u

114 urvive in both the environment and the host, P. aeruginosa must cope with redox stress.

115 hese results shed light on how mucus impacts P. aeruginosa behavior, and may inspire novel approaches

116 In P. aeruginosa, a primary mechanism for protection from r

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

118 ogenesis can also trigger T6SS activation in P. aeruginosa Specifically, we developed a CRISPR interf

119 cholerae can induce T6SS dynamic activity in P. aeruginosa when delivered to or expressed in the peri

120 duces a decrease in the activity of ClpXP in P. aeruginosa, an effect which was also achieved by the

121 on (L154) and antibiotic tolerance (D105) in P. aeruginosa virulence.

122 osynthesis and, thus, for denitrification in P. aeruginosa These three genes here are called ubiT(Pa)

123 at are based on resistance gene detection in P. aeruginosa, acknowledging that such decisions are imp

124 like activator, controls exlBA expression in P. aeruginosa.

125 sine-flipping mechanism is uniquely found in P. aeruginosa TrmD and renders the enzyme inaccessible t

126 etic biology constructs to identify genes in P. aeruginosa and other organisms that enhance electroge

127 plementary data regarding the role of GSH in P. aeruginosa during mammalian infection.

128 rial cell wall assembly and is implicated in P. aeruginosa virulence, yet few studies have addressed

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

130 anding the role of the CF lung microbiome in P. aeruginosa evolution.

131 amase and serine-carbapenemase production in P. aeruginosa The mCIM test was performed according to C

132 type of exclusion mediated by a prophage in P. aeruginosa IMPORTANCE Pseudomonas aeruginosa is a Gra

133 plausible evolutionary trajectory for QS in P. aeruginosa CF infections where LasR mutants arise dur

134 ol of virulence and antibiotic resistance in P. aeruginosa We found that a P. aeruginosa strain lacki

135 ls to virulence and antibiotic resistance in P. aeruginosa.

136 Dismed2 domain of the sensor kinase RetS in P. aeruginosa.

137 GSH plays an important role in P. aeruginosa physiology and is known to modulate severa

138 s were found to have evolved specifically in P. aeruginosa and nearly each species carries different

139 switching from early to middle substrates in P. aeruginosa.

140 of four strains was typically sufficient in P. aeruginosa to converge on a set of core essential gen

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

142 dies into the complex role of CDI systems in P. aeruginosa pathogenesis.

143 sed a similar remodeling of the BfmRS TCS in P. aeruginosa This study highlights the plasticity of TC

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

145 nilate metabolism and bacterial virulence in P. aeruginosa.

146 ent transcripts that RsmA associates with in P. aeruginosa We also find that the RNA chaperone Hfq ta

147 to quantify the virulence of 100 individual P. aeruginosa bloodstream isolates and performed whole-g

148 During intraperitoneal P. aeruginosa infection, phosphorylated hexa-acyl disacc

149 and 14 days using a model of intraperitoneal P. aeruginosa infection.

150 From 95 isogenic P. aeruginosa mutant, an hmgA mutant generated the highe

151 To our knowledge, P. aeruginosa was not previously known to detect and res

152 nd wild-type littermates with the laboratory P. aeruginosa strain PAO1 and CF clinical isolates and t

153 er clinically relevant organisms: M. leprae, P. aeruginosa and S. aureus, despite weak sequence ident

154 enge, particularly in tuberculosis, leprosy, P. aeruginosa and S. aureus infections, where it develop

155 lic recruitment to corneal infections limits P. aeruginosa biofilms to the outer eye surface, prevent

156 ive cell surface receptor for uptake of live P. aeruginosa However, how bacterial motility alters dir

157 omycin + IV meropenem groups presented lower P. aeruginosa concentrations versus amikacin and fosfomy

158 Lung P. aeruginosa burden varied among groups (p < 0.001).

159 o the CF lung abrogate T6SS activity, making P. aeruginosa and its human host susceptible to potentia

160 target for antibiotics development to manage P. aeruginosa infections.

161 In this manner, P. aeruginosa would impair host translation and block an

162 tion (from 3.33 to 2.47 per 10,000), and MDR P. aeruginosa infection (from 13.10 to 9.43 per 10,000),

163 xicillin, and tetracycline, highlighting MDR P. aeruginosa strains of potential public health concern

164 m antibiotics show promise in overcoming MDR P. aeruginosa and are worthy of additional study and dev

165 therapeutic hope against infection with MDR P. aeruginosa that lack metallo-beta-lactamases.

166 ical significance of P. aeruginosa, modeling P. aeruginosa infections in CF has been challenging.

167 ates the uptake of both motile and nonmotile P. aeruginosa However, unexpectedly, mechanistic studies

168 In these U.S. hospital ICUs, carbapenem-NS P. aeruginosa isolates from respiratory sources were fre

169 inosa and Staphylococcus aureus, we observed P. aeruginosa can modify surface motility in response to

170 ng successfully categorized 91% (112/123) of P. aeruginosa isolates as carbapenemases or non-carbapen

171 Pyocins are produced by more than 90% of P. aeruginosa strains and may have utility as last resor

172 found in matrix EPS and mediate adherence of P. aeruginosa to target host cells.

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

174 Pyocins, bacteriocins of P. aeruginosa, are potent and diverse protein antibiotic

175 proteins promote uptake, but not binding, of P. aeruginosa by murine neutrophils, which supports a ro

176 In the case of P. aeruginosa, the effector protein ExoS is central to l

177 erneath them two catheters with 10(5) CFU of P. aeruginosa before the surgical wounds were hermetical

178 burn wounds inoculated with 1 x 10(4) CFU of P. aeruginosa.

179 Adaptive metabolic changes of P. aeruginosa were generally required during both infect

180 ility of a large international collection of P. aeruginosa isolates (n = 198) to fosfomycin and to co

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

182 stable platform for the rapid comparison of P. aeruginosa isolates using whole-genome sequencing (WG

183 sets the stage for light-mediated control of P. aeruginosa infectivity.

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

185 nstrated to be required for the formation of P. aeruginosa biofilms, we asked whether pyruvate likewi

186 lginate and pellicle biofilm matrix genes of P. aeruginosa within the burn eschar.

187 vaT and MvaU may contribute to the growth of P. aeruginosa.

188 Therefore, DMBT1 inhibition of P. aeruginosa twitching motility involves its N-glycosyl

189 Isolation of P. aeruginosa with new resistance to antipseudomonal dru

190 Since the denitrification metabolism of P. aeruginosa is believed to be important for the pathog

191 ial load and inflammation in mouse models of P. aeruginosa intraperitoneal and respiratory infection.

192 3 presented a net reduction in the number of P. aeruginosa on the surface of the foreign body and les

193 of the enzymatically active soluble part of P. aeruginosa AlgC in 1991, all subsequent studies utili

194 The pathogenicity of P. aeruginosa is dependent on quorum sensing (QS), an in

195 that cigarette smoke alters the phenotype of P. aeruginosa, increasing virulence and making it less s

196 udy, a significant decrease in prevalence of P. aeruginosa (P < 0.001) and S. aureus (P < 0.001) was

197 The decrease in prevalence of P. aeruginosa and S. aureus since 2000, coinciding with

198 y, we analysed the transcriptomic profile of P. aeruginosa cells isolated from lungs of infected mice

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

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

201 We also studied the role of P. aeruginosa GSH biosynthesis in four mouse infection m

202 Despite the clinical significance of P. aeruginosa, modeling P. aeruginosa infections in CF h

203 trated that the oxygen levels at the site of P. aeruginosa infection can strongly influence virulence

204 hat the gallbladder is crucial for spread of P. aeruginosa from the bloodstream to the feces during b

205 letion mutants of two independent strains of P. aeruginosa and with CRISPR-generated CD18-deficient c

206 Antibiotic resistance in multiple strains of P. aeruginosa is a rapidly developing clinical problem.

207 llonella larvae infected with MDR strains of P. aeruginosa.

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

209 li Here, we present the crystal structure of P. aeruginosa IGPS in complex with reduced CdRP, a nonre

210 rn operon led to increased susceptibility of P. aeruginosa to AZM and great increases in synergy betw

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

212 er understand the evolutionary trajectory of P. aeruginosa QS in chronic infections, we grew LasR mut

213 cillin-tazobactam as definitive treatment of P. aeruginosa bacteremia.

214 a complementary approach in the treatment of P. aeruginosa infection.

215 RNA-Seq analyses upon treatment of P. aeruginosa with AB569 revealed a catastrophic loss of

216 which was also achieved by the treatment of P. aeruginosa with N-acetylglucosamine (GlcNAc), a wides

217 In particular, treatment of P. aeruginosa with sublethal concentrations of antibioti

218 l strategies for prevention and treatment of P. aeruginosa-induced pneumonia and subsequent ARDS.

219 work that has advanced our understanding of P. aeruginosa infection.

220 nts for phagocytic recognition and uptake of P. aeruginosa.

221 al transcriptional analysis was performed on P. aeruginosa with and without effective concentrations

222 Only P. aeruginosa and Aspergillus were associated with progr

223 ore susceptible to infection by S. aureus or P. aeruginosa, resulting in increased mortality and orga

224 netic experiments indicating that E. coli or P. aeruginosa strains that lack cardiolipin synthase are

225 over, seven of eight Bcc strains outcompeted P. aeruginosa strains isolated from the same patients.

226 inally, inhibition of inflammasome prevented P. aeruginosa-induced acute lung injury.

227 mical inhibition and ENT1 knockout prevented P. aeruginosa-induced lung NLRP3 inflammasome activation

228 Identification of carbapenemase-producing P. aeruginosa will have therapeutic, epidemiological, an

229 e mutants are surrounded by C4-HSL-producing P. aeruginosa, variants rewired to have a LasR-independe

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

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

232 Purified P. aeruginosa Mhr protein contained the predicted di-iro

233 cin and fosfomycin alone efficiently reduced P. aeruginosa in tracheal secretions, with negligible ef

234 autions as contributory factors for reducing P. aeruginosa (Pa) infections in intensive care units (I

235 patients infected with carbapenem-resistant P. aeruginosa isolates susceptible to TOL-TAZ and treate

236 Carbapenem-resistant P. aeruginosa NCTC 13437 and an unrelated clinical isola

237 myxins or aminoglycosides for drug-resistant P. aeruginosa infections.

238 egimens for infections due to drug-resistant P. aeruginosa.

239 Higher rates of resistant P. aeruginosa after patients were treated with carbapene

240 complement-mediated lysis of serum-resistant P. aeruginosa strains, indicating the importance of an i

241 We searched P. aeruginosa genomes from collections available from se

242 Here, we show P. aeruginosa isolates from teenage and adult CF patient

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

244 that interfere specifically with late-stage P. aeruginosa development.

245 ns, we grew LasR mutants of the well-studied P. aeruginosa strain, PAO1, in conditions that recapitul

246 ftazidime-avibactam (CAZ-AVI) had subsequent P. aeruginosa isolates with high-level resistance to CAZ

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

248 uilibrium after 3 h, a time much longer than P. aeruginosa duplication time.

249 These findings demonstrate that P. aeruginosa QS molecules may confer protection to neig

250 We observed that P. aeruginosa (strain: PA103) infection induced acute lu

251 Here, we report that P. aeruginosa PAO1 produced sulfane sulfur, including gl

252 We report that P. aeruginosa upregulates expression of heme uptake mach

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

254 rio cholerae (random-firing), revealing that P. aeruginosa does indeed fire multiple times per incomi

255 we use a mouse infection model to show that P. aeruginosa can spread from the bloodstream to the gal

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

257 aken together, our observations suggest that P. aeruginosa deploys a virulence mechanism to induce ri

258 The P. aeruginosa genome encodes two heme uptake systems, th

259 The P. aeruginosa PPA and NPA, respectively, were 95.9% (88.

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

261 o be the most potent virulence factor in the P. aeruginosa arsenal, and also elevated expression of t

262 directly correlated with the density of the P. aeruginosa population and required viable P. aerugino

263 ulator of the expression and activity of the P. aeruginosa Type I-F CRISPR-Cas system.

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

265 Molecules that interact with the P. aeruginosa outer membrane such as polymyxin B can als

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

267 We found that upon exposure to P. aeruginosa PA14, C. elegans undergoes a rapid loss of

268 and that this association is not limited to P. aeruginosa This is to be contrasted with chronic resp

269 roperties, is not upregulated in response to P. aeruginosa by cystic fibrosis airway epithelia.

270 nd M1-macrophage polarization in response to P. aeruginosa pneumonia in vitro and in vivo.

271 nd improve the epithelial innate response to P. aeruginosa.

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

273 4(-/-) mice from increased susceptibility to P. aeruginosa pneumonia.

274 l SagS to be a promising new target to treat P. aeruginosa biofilm infections.

275 (2)), which is higher than that of wild-type P. aeruginosa and even the strongly electrogenic organis

276 ed the proteome of three different wild-type P. aeruginosa strains, their eftM mutants, and these mut

277 he effects of RpoN* on phenotypically varied P. aeruginosa strains isolated from CF patients.

278 P. aeruginosa population and required viable P. aeruginosa bacteria.

279 H69 cleavage is elicited by certain virulent P. aeruginosa isolates in a quorum sensing (QS)-dependen

280 (CDI) system enriched among highly virulent P. aeruginosa isolates.

281 When P. aeruginosa is transferred daily on casein, QS mutants

282 Here, we describe a new phenomenon by which P. aeruginosa tolerates antibiotic treatment.

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

284 While P. aeruginosa can initiate long-term infections in young

285 Enterobacterales, whereas it was 96.0% with P. aeruginosa The MCR-1 LFA and EDTA-CBDE methods are bo

286 predominant virulence genes associated with P. aeruginosa infection.

287 y/mass spectrometry as being associated with P. aeruginosa infection.

288 ophilia formed well-integrated biofilms with P. aeruginosa, and these organisms colocalize in the lun

289 ecificities and interact differentially with P. aeruginosa ClpX and ClpA.

290 Experimentally infected fish with P. aeruginosa displayed high mortalities in direct propo

291 cine second-degree burn wounds infected with P. aeruginosa biofilm cells, we furthermore demonstrated

292 d with IFN-gamma or IL-17A and infected with P. aeruginosa The intent of this design was to model (i)

293 Importantly, polymicrobial infection with P. aeruginosa elicited significantly higher S. maltophil

294 sted with chronic respiratory infection with P. aeruginosa, suggesting that either the chronicity or

295 mouse model of subcutaneous inoculation with P. aeruginosa, rTCP96 reduced bacterial levels.

296 mortality when challenged intranasally with P. aeruginosa.

297 s aureus, a common pathogen co-isolated with P. aeruginosa from polymicrobial human infections.

298 macrophages expressed FABP4 in WT mice with P. aeruginosa pneumonia.

299 rs) including 767 hospitalized patients with P. aeruginosa bacteremia treated with beta-lactam monoth

300 te treatment primarily impacts patients with P. aeruginosa-related BSI mortality and in turn is the o