ライフサイエンスコーパス: B. pseudomallei

1 B. pseudomallei capsular polysaccharide (CPS) I comprise

2 B. pseudomallei expresses three serologically distinct L

3 B. pseudomallei FliC contained several peptide sequences

4 B. pseudomallei induced lower monocyte-normalized levels

5 B. pseudomallei infection rapidly generated a potent IFN

6 B. pseudomallei is a facultative intracellular pathogen

7 B. pseudomallei is an encapsulated bacterium that can in

8 B. pseudomallei is classed as a tier 1 select agent by t

9 B. pseudomallei isolates from the property's groundwater

10 B. pseudomallei locus tags within the full text and tabl

11 B. pseudomallei mutant strains lacking components of the

12 B. pseudomallei was associated with a high soil water co

13 mallei proteins, and new information for 281 B. pseudomallei proteins associated with 5 secretion sys

14 We used whole genome sequences of 469 B. pseudomallei isolates from 30 countries collected ove

15 We sequenced the 1.5-kb 16S rRNA gene of 56 B. pseudomallei and 23 B. mallei isolates selected to re

16 s across additional genome sequences and 571 B. pseudomallei DNA extracts obtained from regions of en

17 98 virulence attenuation experiments for 61 B. pseudomallei secretion system proteins.

18 restore the actin-based motility defect of a B. pseudomallei bimA mutant.

19 tudy, we characterized the interactions of a B. pseudomallei bsaZ mutant with RAW 264.7 murine macrop

20 mallei strains successfully hybridize with a B. pseudomallei strain not used for probe design.

21 nd computationally derived information about B. pseudomallei K96243.

22 atabase with corresponding information about B. pseudomallei.

23 ne-induced protective immunity against acute B. pseudomallei infection.

24 upregulates the expression of ~30 additional B. pseudomallei genes, including some that may confer pr

25 ALB/c mice to various amounts of aerosolized B. pseudomallei 1026b to determine lethality.

26 en monkeys (AGMs) was exposed to aerosolized B. pseudomallei 1026b.

27 After low-dose inoculation with aerosolized B. pseudomallei, Nod2-deficient mice showed impaired cli

28 rrogates of antigen-induced immunity against B. pseudomallei as well as provide valuable insights tow

29 itutes effective protective immunity against B. pseudomallei infection remains incomplete.

30 ctive cell mediated immune responses against B. pseudomallei, but may also moderate the pathological

31 nt genetic manipulation of the select agents B. pseudomallei and B. mallei using allelic exchange.

32 Nearly all B. pseudomallei strains sequenced to date (> 85 isolates

33 hat genomic islands (GIs) vary greatly among B. pseudomallei strains.

34 B. mallei and B. pseudomallei are closely related genetically; B. mall

35 Burkholderia mallei and B. pseudomallei are important human pathogens and cause

36 Burkholderia mallei and B. pseudomallei are the causative agents of glanders and

37 Burkholderia mallei and B. pseudomallei cause glanders and melioidosis, respecti

38 genic mechanisms of action for B. mallei and B. pseudomallei secretion system proteins inferred from

39 gned to identify all Burkholderia mallei and B. pseudomallei strains successfully hybridize with a B.

40 of protective immunity against B. mallei and B. pseudomallei, including antigen discovery.

41 secretion system proteins for B. mallei and B. pseudomallei, their pathogenic mechanisms of action,

42 enge with 100% lethal doses of B. mallei and B. pseudomallei.

43 from aerosol exposure to both B. mallei and B. pseudomallei.

44 tifying unsequenced strains of B. mallei and B. pseudomallei.

45 ion about secretion systems of B. mallei and B. pseudomallei.

46 supernatants of B. pseudomallei MSHR668 and B. pseudomallei DeltagspD grown in rich and minimal medi

47 for B. anthracis and <6 h for Y. pestis and B. pseudomallei One exception was B. pseudomallei in the

48 50% to 75% for B. anthracis, Y. pestis, and B. pseudomallei compared to conventional methods.

49 f mice treated with doxycycline survived and B. pseudomallei DNA was not amplified from the lungs or

50 m lethal challenge with B. thailandensis and B. pseudomallei.

51 No coworkers had detectable anti-B. pseudomallei antibody, whereas seropositive results a

52 We assessed B. pseudomallei FliC peptide binding affinity to multipl

53 There is currently no attenuated B. pseudomallei strain available that is excluded from s

54 n apparatus (Bsa) in the interaction between B. pseudomallei and host cells.

55 ated to investigate cross-reactivity between B. pseudomallei and the related Burkholderia species ass

56 melioidosis, an infectious disease caused by B. pseudomallei, is diabetes mellitus.

57 during severe Gram-negative sepsis caused by B. pseudomallei.

58 We measured NF-kappaB activation induced by B. pseudomallei in human embryonic kidney-293 cells tran

59 OD2 mediated NF-kappaB activation induced by B. pseudomallei stimulation of HEK293 cells.

60 was the only Hcp constitutively produced by B. pseudomallei in vitro; however, it was not exported t

61 ations suggest that some factors required by B. pseudomallei for resistance to environmental phagocyt

62 0 putative virulence-related genes shared by B. pseudomallei and B. mallei but not present in five cl

63 vement was essential for cell-cell spread by B. pseudomallei and B. thailandensis, neither BimA-media

64 of VgrG5 facilitates intercellular spread by B. pseudomallei and related species following injection

65 ells were pulsed with heat-killed whole-cell B. pseudomallei and used to immunize syngeneic mice.

66 We observed that primary clinical B. pseudomallei isolates with mucoid and nonmucoid colon

67 In contrast, B. pseudomallei and B. mallei BimA mimic host Ena/VASP a

68 In contrast, B. pseudomallei-specific CD4(+) T cells played an import

69 nd neutrophils are important for controlling B. pseudomallei infections, however few details are know

70 growth characteristics of a recently created B. pseudomallei 1026b Deltaasd mutant in vitro, in a cel

71 have shown that BipC was capable of delayed B. pseudomallei actin-based motility.

72 e. 25 x 25 m) should be sufficient to detect B. pseudomallei at a given location if samples are taken

73 for rapidly identifying and differentiating B. pseudomallei and B. mallei by molecular methods.

74 a useful diagnostic tool for differentiating B. pseudomallei and B. mallei, two closely related biolo

75 retion system gene cluster and distinguishes B. pseudomallei from other microbial species.

76 phically, temporally, and clinically diverse B. pseudomallei isolates from the Centers for Disease Co

77 rsor biliverdin, ferrous iron, and CO during B. pseudomallei infection.

78 imal cases and the presence of environmental B. pseudomallei and combine this in a formal modelling f

79 mal cases, and the presence of environmental B. pseudomallei, and combine this in a formal modelling

80 o, suggesting that BPSS1823 is important for B. pseudomallei virulence.

81 cultured soil from a rice field in Laos for B. pseudomallei at different depths on 4 occasions over

82 Approved markers for B. pseudomallei include genes encoding resistance to kan

83 ter than the 30 cm currently recommended for B. pseudomallei environmental sampling.

84 Empiric use of antibiotics not specific for B. pseudomallei was associated with increased risk of de

85 ealing with clinical isolates suspicious for B. pseudomallei or clinical specimens from suspected mel

86 rapidly recognizing isolates suspicious for B. pseudomallei, be able to safely perform necessary rul

87 Presently, there is no licensed vaccine for B. pseudomallei and the organism is refractive to antibi

88 oxyheptan capsular polysaccharide (CPS) from B. pseudomallei was purified, chemically activated, and

89 iA-CT(E479) is another CDI toxin domain from B. pseudomallei 1026b.

90 4 as a model, we show that a CDI system from B. pseudomallei 1026b mediates CDI and is capable of del

91 of AhpC is virtually invariant among global B. pseudomallei clinical isolates, a Cambodian isolate v

92 The FCR method showed greater B. pseudomallei detection sensitivity than conventional

93 0 host-B. mallei interactions and 2,286 host-B. pseudomallei interactions.

94 T cell hybridomas against an immunogenic B. pseudomallei FliC epitope also cross-reacted with ort

95 CPS I improved B. pseudomallei survival in vivo and triggered multiple

96 Deficiency of Nrf2 improved B. pseudomallei clearance by macrophages, whereas Nrf2 a

97 nce gene expression and stress adaptation in B. pseudomallei, and the DeltarelA DeltaspoT mutant may

98 open reading frame Bp1026b_II1054 (bcaA) in B. pseudomallei strain 1026b is predicted to encode a cl

99 strain generated by deletion of BPSS1823 in B. pseudomallei exhibited a reduced ability to survive w

100 ction of a group 3 polysaccharide capsule in B. pseudomallei is essential for virulence.

101 Orthologs of these genes were disrupted in B. pseudomallei, and nearly all mutants had similarly de

102 n to encompass strong CD4 T cell epitopes in B. pseudomallei-exposed individuals and in HLA transgeni

103 identify high-probability virulence genes in B. pseudomallei, B. mallei, and other pathogens.

104 ely, these findings show a role for CPS I in B. pseudomallei survival in vivo following inhalation in

105 Nine 16S types were identified in B. pseudomallei isolates based on six positions of diffe

106 ograms targeting both at-risk individuals in B. pseudomallei endemic regions as well as CF patients.

107 ates flagellar glycosylation and motility in B. pseudomallei.

108 udy, we created a relA spoT double mutant in B. pseudomallei strain K96243, which lacks (p)ppGpp-synt

109 te multiple unmarked and in-frame mutants in B. pseudomallei, and one mutant in B. mallei.

110 S genes may be remnants of the QS network in B. pseudomallei from which this host-adapted pathogen ev

111 y contribute to the pathogenesis observed in B. pseudomallei infection.

112 (e.g. PenA in B. cepacia complex and PenI in B. pseudomallei).

113 s involved in LPS synthesis was performed in B. pseudomallei K96243.

114 dosis, suggesting a role for type IV pili in B. pseudomallei virulence.

115 rbohydrate covalently linked to a protein in B. pseudomallei and B. thailandensis, and it suggests ne

116 e show that the homologous genomic region in B. pseudomallei strain 305 is similar to that previously

117 We have named this region in B. pseudomallei strain 305 the B. thailandensis-like fla

118 Here, we identify 10 distinct CDI systems in B. pseudomallei based on polymorphisms within the cdiA-C

119 rt that inactivating gmhA, wcbJ, and wcbN in B. pseudomallei K96243 retains the immunogenic integrity

120 t model system for facilitating inquiry into B. pseudomallei virulence.

121 down reduced the survival of intramacrophage B. pseudomallei Pharmacological administration of cobalt

122 vity results guided soil sampling to isolate B. pseudomallei.

123 In summary, neutrophils can efficiently kill B. pseudomallei and B. thailandensis that possess a crit

124 oduction induced by flagellin or heat-killed B. pseudomallei by TLR5(1174C)>T genotype in healthy sub

125 econd dose of dendritic cells or heat-killed B. pseudomallei were administered to increase the immune

126 se relatives with very different lifestyles: B. pseudomallei is an opportunistic pathogen, B. thailan

127 roxidase (GPx) of PMNs after exposed to live B. pseudomallei.

128 Mice were intranasally infected with live B. pseudomallei and killed after 24, 48, or 72 hours for

129 ated diabetic individuals infected with live B. pseudomallei in vitro showed lower free glutathione (

130 h genome sequences are available, B. mallei, B. pseudomallei, and B. cepacia, are predicted to contai

131 Moreover, B. pseudomallei encodes proteins that are very similar t

132 -results and decrease the number of negative B. pseudomallei reports that are currently observed from

133 n (BimA) that is required for the ability of B. pseudomallei to induce the formation of actin tails.

134 to play an important role in the ability of B. pseudomallei to survive and replicate in mammalian ce

135 basis of this structure and the activity of B. pseudomallei GmhA mutants.

136 at alkyl hydroperoxidase reductase (AhpC) of B. pseudomallei is strongly immunogenic for T cells of '

137 ntigen and culture filtrate [CF] antigen) of B. pseudomallei The ELISAs were evaluated using serum sa

138 little is known about the molecular basis of B. pseudomallei pathogenicity, in part because of the la

139 in modulating the intracellular behaviour of B. pseudomallei.

140 the role of these systems in the biology of B. pseudomallei.

141 entified calprotectin as a lead biomarker of B. pseudomallei infections and examined correlations bet

142 We report the capacity of B. pseudomallei to enter, efficiently replicate in, and

143 However, culture of B. pseudomallei in environmental samples is difficult an

144 We used aerosol delivery of B. pseudomallei to establish respiratory infection in mi

145 nd Bp190, which are DeltapurM derivatives of B. pseudomallei strains 1026b and K96243 that are defici

146 fungi, MB bottles improved the detection of B. pseudomallei (27% [MB] versus 8% [F]; P < 0.0001), wi

147 Detection of B. pseudomallei DNA or recovery of the pathogen by cultu

148 S1PL as a critical virulence determinant of B. pseudomallei and B. thailandensis, further highlighti

149 tis was the central step in dissemination of B. pseudomallei from the lungs as well as in the establi

150 The global distribution of B. pseudomallei and burden of melioidosis, however, rema

151 The global distribution of B. pseudomallei and the burden of melioidosis, however,

152 nce for the rapid in vivo diversification of B. pseudomallei after inoculation and systemic spread.

153 rates when challenged with a lethal dose of B. pseudomallei.

154 ly infected with either high or low doses of B. pseudomallei to generate either acute, chronic, or la

155 iew, unique and shared virulence features of B. pseudomallei and B. mallei are discussed.

156 lso contribute to the competitive fitness of B. pseudomallei.

157 that the protein encoded by the BipD gene of B. pseudomallei is an important secreted virulence facto

158 The genome of B. pseudomallei strain 1026b encodes nine putative trime

159 y identified in comparisons of the genome of B. pseudomallei strain K96243 with the genome of strain

160 of endogenous sacBC genes in the genomes of B. pseudomallei and B. mallei.

161 say is a valuable tool for identification of B. pseudomallei and may improve diagnosis in regions end

162 CR for rapid and sensitive identification of B. pseudomallei that has been tested for cross-reactivit

163 South American isolates with introduction of B. pseudomallei into the Americas between 1650 and 1850,

164 ty between two distinct clinical isolates of B. pseudomallei, 1026b and K96243.

165 Taken together, isolation of B. pseudomallei from a soil sample and high seropositivi

166 healthy individuals and improved killing of B. pseudomallei in vitro.

167 rtant role in the intracellular lifestyle of B. pseudomallei.

168 The subcellular location of B. pseudomallei within infected RAW 264.7 cells was dete

169 greatly hampered the genetic manipulation of B. pseudomallei and B. mallei and currently few reliable

170 nt compliant for the genetic manipulation of B. pseudomallei and B. mallei.

171 elect Agent-excluded purM deletion mutant of B. pseudomallei (strain Bp82) and then subjected to intr

172 The unfavorable outcome of B. pseudomallei infection after HO-1 induction was assoc

173 of 45 SSH-derived sequences among a panel of B. pseudomallei and B. thailandensis isolates.

174 niches and contribute to the pathogenesis of B. pseudomallei and B. mallei.

175 roteins, but its role in the pathogenesis of B. pseudomallei infection is not well understood.

176 o-chemical associations with the presence of B. pseudomallei.

177 A higher prevalence of B. pseudomallei was found at soil depths greater than th

178 The secretion profiles of B. pseudomallei MSHR668 and its T2SS mutants were notice

179 This global survey of the QS regulons of B. pseudomallei, B. thailandensis, and B. mallei serves

180 ht into a frequently overlooked reservoir of B. pseudomallei.

181 developed to monitor levels of resistance of B. pseudomallei and the closely related nearly avirulent

182 The genomic sequence of B. pseudomallei K96243 was recently determined, but litt

183 virulence with roles in different stages of B. pseudomallei pathogenesis, including extracellular an

184 A bipC TTSS-3-deficient strain of B. pseudomallei and complemented strains were generated

185 . mallei evolved from an ancestral strain of B. pseudomallei by genome reduction and adaptation to an

186 pathogenic, select-agent-excluded strains of B. pseudomallei and covalently linked to carrier protein

187 Genomic differences among strains of B. pseudomallei are predicted to be one of the major cau

188 DNA from eight strains of B. pseudomallei that were spiked into synthetic urine at

189 ed GIs are common across multiple strains of B. pseudomallei.

190 ctive immune responses to various strains of B. pseudomallei.

191 enome sequences of five reference strains of B. pseudomallei: K96243, 1710b, 1106a, MSHR668, and MSHR

192 pared the genome sequences of two strains of B. pseudomallei: the original reference strain K96243 fr

193 tify proteins present in the supernatants of B. pseudomallei MSHR668 and B. pseudomallei DeltagspD gr

194 protein in the type-III secretion system of B. pseudomallei.

195 Due to the potential malicious use of B. pseudomallei as well as its impact on public health i

196 to determine its role(s) in the virulence of B. pseudomallei pathogenesis.

197 sequences of 15 strains of B. oklahomensis, B. pseudomallei, B. thailandensis, and B. ubonensis to a

198 with the NOD2 ligand, muramyl dipeptide, or B. pseudomallei.

199 delivering CdiA-CT toxins derived from other B. pseudomallei strains.

200 Thus, the T cell response to primary B. pseudomallei infection is biphasic, an early cytokine

201 e proteins exported by these systems provide B. pseudomallei with a growth advantage in vitro and in

202 with a combination of CPS2B1 and recombinant B. pseudomallei LolC, rather than with CPS2B1 or LolC in

203 used to prepare highly purified recombinant B. pseudomallei Hcp1 and TssM proteins.

204 A total of 266 Thai B. pseudomallei isolates were characterized (83 soil and

205 landensis was more readily phagocytosed than B. pseudomallei, but both displayed similar rates of per

206 ed significantly more C3 on its surface than B. pseudomallei, whose polysaccharide capsule significan

207 Based upon these findings, it appears that B. pseudomallei may not require T3SS-1, -2, and -3 to fa

208 We demonstrate that B. pseudomallei down-regulation of ELT-2 targets is asso

209 wo strains of each species demonstrated that B. pseudomallei flagellin proteins were modified with a

210 resonance (NMR) spectroscopy, we found that B. pseudomallei 4095a and 4095c OPS antigens exhibited s

211 evaluated as a surrogate host; we found that B. pseudomallei and B. mallei, but not other phylogeneti

212 3 cells transfected with TLR5 and found that B. pseudomallei induced TLR5(1174C)- but not TLR5(1174T)

213 We found that B. pseudomallei-infected PBMCs from diabetic patients we

214 Our studies indicate that B. pseudomallei OPS undergoes antigenic variation and su

215 Furthermore, we show that B. pseudomallei invades fibroblasts and keratinocytes an

216 Recent studies have shown that B. pseudomallei Bsa type III secretion system 3 (T3SS-3)

217 The results presented here suggest that B. pseudomallei strains are genetically heterogeneous an

218 The B. pseudomallei DeltarelA DeltaspoT mutant displayed a d

219 The B. pseudomallei flagellar protein FliC is strongly seror

220 wn TTSS effectors from other bacteria in the B. pseudomallei genome.

221 e CO-releasing molecule CORM-2 increases the B. pseudomallei load in macrophages and mice.

222 of mono- and disaccharidic fragments of the B. pseudomallei and B. mallei CPS repeating unit is repo

223 Further characterization of the B. pseudomallei Deltaasd mutant revealed a marked decrea

224 Human OECs killed >90% of the B. pseudomallei in a CPS I-independent manner and exhibi

225 s the first in-depth characterization of the B. pseudomallei T2SS secretome.

226 ts a 115-base-pair region within orf2 of the B. pseudomallei type III secretion system gene cluster a

227 Degradation of ELT-2 requires the B. pseudomallei type III secretion system.

228 Thus, our data suggest that the B. pseudomallei-mediated induction of HO-1 and the relea

229 One of these, the B. pseudomallei T3SS2 (T3SS2(bp)) gene cluster, which ap

230 Thus, the B. pseudomallei Deltaasd mutant may be a promising live

231 Mice immunized with the B. pseudomallei K96243 mutants lacking a functional copy

232 that a triple mutant defective in all three B. pseudomallei T3SSs exhibited the same phenotype as th

233 Biochemical analysis of three B. pseudomallei CdiA-CTs revealed that each protein poss

234 luxR homologs, and these genes contribute to B. pseudomallei and B. mallei virulence.

235 ere tested for evidence of prior exposure to B. pseudomallei by indirect hemagglutination assay.

236 Following exposure to B. pseudomallei, mice lacking the lectin-like domain of

237 he susceptibility of diabetic individuals to B. pseudomallei infection.

238 rther explore the role of the OM response to B. pseudomallei infection, we infected human olfactory e

239 mide on GSH and PMN functions in response to B. pseudomallei that may contribute to the susceptibilit

240 d feature of the transcriptional response to B. pseudomallei was a progressive increase in the propor

241 contribution of NOD2 to the host response to B. pseudomallei.

242 insights into the host defense responses to B. pseudomallei infection within an intact host, we anal

243 to induce cell-mediated immune responses to B. pseudomallei.

244 mice demonstrated enhanced susceptibility to B. pseudomallei infection compared with wild type mice a

245 o identify sequences that varied between two B. pseudomallei isolates from Australia and determined t

246 Although unrelated in sequence, the two B. pseudomallei nuclease domains share similar folds and

247 n (Gm), and zeocin (Zeo); however, wild type B. pseudomallei is intrinsically resistant to these anti

248 formation, which were observed in wild-type B. pseudomallei cell infections.

249 Mutational analysis of wild-type B. pseudomallei demonstrated that ceftazidime resistance

250 bcaA and Bp340DeltabcaB mutants to wild-type B. pseudomallei in vitro demonstrated similar levels of

251 ant levels of protection against a wild-type B. pseudomallei K96243 challenge.

252 ve immunity against challenge with wild-type B. pseudomallei, suggesting that the genes identified in

253 protection against infection with wild-type B. pseudomallei.

254 se of 6,000 median lethal doses of wild-type B. pseudomallei.

255 Hybridization results with an unsequenced B. pseudomallei strain indicate that the designed probes

256 Mutagenesis and secretion experiments using B. pseudomallei strains engineered to express T6SS-5 in

257 sitivity of detection and recovery of viable B. pseudomallei cells from small volumes (0.45 ml) of ur

258 Mice were intranasally infected with viable B. pseudomallei and killed after 24, 48, or 72 hours for

259 comparable to signaling induced by virulent B. pseudomallei.

260 animals were challenged with fully virulent B. pseudomallei, and protection was demonstrated in thos

261 human neutrophils to control highly virulent B. pseudomallei compared to the relatively avirulent, ac

262 jected to intranasal challenge with virulent B. pseudomallei strain 1026b.

263 pestis and B. pseudomallei One exception was B. pseudomallei in the presence of ceftazidime, which re

264 ed by a later antigen-induced phase in which B. pseudomallei-specific T cells, in particular CD4(+) T

265 urvived a lethal inhalational challenge with B. pseudomallei Remarkably, 70% of the survivors had no

266 Upon virulent challenge with B. pseudomallei strain K96243, NCTC 4845, or 576, animal

267 d significant protection from challenge with B. pseudomallei, and protection was associated with a si

268 ected against intraperitoneal challenge with B. pseudomallei.

269 Thailand was co-cultured with B. pseudomallei and production of IL-10 and IFN-gamma de

270 P(-/-)) mice were intranasally infected with B. pseudomallei to induce severe pneumosepsis (melioidos

271 ogenates were elevated in mice infected with B. pseudomallei.

272 and fungal infections and for infection with B. pseudomallei, a common cause of septicemia in Thailan

273 Human infections with B. pseudomallei (called melioidosis) present as a range

274 develop chronic, subclinical infections with B. pseudomallei.

275 ibiotics and capacity for latency, work with B. pseudomallei requires a biosafety level 3 (BSL-3) con

276 he major sources of genomic diversity within B. pseudomallei and the molecular mechanisms that facili

277 mic states define two distinct groups within B. pseudomallei: all strains contained either the BTFC g

278 Overall, 195 of 653 samples (29.7%) yielded B. pseudomallei.