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 carries a putative cyclophilin B gene, p

3 B. pseudomallei expresses three serologically distinct L

4 B. pseudomallei FliC contained several peptide sequences

5 B. pseudomallei induced lower monocyte-normalized levels

6 B. pseudomallei is an encapsulated bacterium that can in

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

8 B. pseudomallei isolates from the property's groundwater

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

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

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

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

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

14 98 virulence attenuation experiments for 61 B. pseudomallei secretion system proteins.

15 A B. pseudomallei DeltappiB (BpsDeltappiB) mutant strain d

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

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

18 nd computationally derived information about B. pseudomallei K96243.

19 atabase with corresponding information about B. pseudomallei.

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

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

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

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

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

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

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

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

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

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

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

31 species: B. thailandensis, B. gladioli, and B. pseudomallei Furthermore, we show that absence of pro

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

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

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

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

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

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

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

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

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

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

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

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

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

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

46 50% to 75% for B. anthracis, Y. pestis, and B. pseudomallei compared to conventional methods.

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

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

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

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

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

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

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

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

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

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

57 ere expressed during macrophage infection by B. pseudomallei K96243.

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

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

60 0 putative virulence-related genes shared by B. pseudomallei and B. mallei but not present in five cl

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

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

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

64 Comparing B. pseudomallei wild-type with plc mutants revealed that

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

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

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

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

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

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

71 dvances in our understanding of the disease, B. pseudomallei poses a significant health risk, especia

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

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

74 d internalization and membrane fusion during B. pseudomallei infection.

75 ainst CD9 and CD9-EC2 significantly enhanced B. pseudomallei internalization, but MAb against CD81 an

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

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

78 and infection induced weight loss following B. pseudomallei infection.

79 ll to cell, indicating ppiB is essential for B. pseudomallei virulence.

80 gen and that type 1 fimbria is important for B. pseudomallei intestinal adherence, and we identify a

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

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

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

84 lysis showed similar LPS ladder patterns for B. pseudomallei, B. thailandensis, and B. mallei, these

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

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

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

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

89 t Burkholderia species and compare those for B. pseudomallei to those for the other seven species.

90 functional characterization of BPSS2242 from B. pseudomallei.

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

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

93 4 as a model, we show that a CDI system from B. pseudomallei 1026b mediates CDI and is capable of del

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

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

96 0 host-B. mallei interactions and 2,286 host-B. pseudomallei interactions.

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

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

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

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

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

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

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

104 ystem against reactive carbonyl compounds in B. pseudomallei..

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

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

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

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

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

110 alysis we have identified 8 putative Ltgs in B. pseudomallei K96243.

111 ates flagellar glycosylation and motility in B. pseudomallei.

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

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

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

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

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

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

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

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

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

121 Their roles in B. pseudomallei infection were investigated in vitro usi

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

123 udy investigated the role of tetraspanins in B. pseudomallei infection.

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

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

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

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

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

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

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

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

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

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

134 th B. cenocepacia, Burkholderia multivorans, B. pseudomallei, or Burkholderia mallei develop O-glycan

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

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

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

138 bria is involved in the initial adherence of B. pseudomallei to IECs, although the impact on full vir

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

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

141 owth kinetics or the levels of bacteremia of B. pseudomallei represent the next-generation of diagnos

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

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

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

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

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

147 signatures obtained from microarray data of B. pseudomallei-infected cases to develop a real-time PC

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

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

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

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

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

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

154 oth ancient and more recent dissemination of B. pseudomallei to Myanmar and elsewhere in Southeast As

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

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

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

158 The diversity of B. pseudomallei from Myanmar and divergence within our g

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

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

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

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

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

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

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

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

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

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

169 ny suggest that the original introduction of B. pseudomallei to Myanmar was not a recent event.

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

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

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

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

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

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

176 derstanding into the molecular mechanisms of B. pseudomallei virulence and dormancy.

177 st notably the dynamic nature of movement of B. pseudomallei within densely populated Southeast Asia.

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

179 ity, phylogeography and potential origins of B. pseudomallei in Myanmar.

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

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

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

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

184 nd open a new avenue for the pathogenesis of B. pseudomallei.

185 rovides new insights into global patterns of B. pseudomallei dissemination, most notably the dynamic

186 es display markedly impaired phagocytosis of B. pseudomallei In conclusion, these data suggest that T

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

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

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

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

191 netic evidence of repeated reintroduction of B. pseudomallei across countries bordered by the Mekong

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

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

194 present the first whole-genome sequences of B. pseudomallei isolates from Myanmar: nine clinical and

195 o bound magnesium ions in the active site of B. pseudomallei OLD in a geometry that supports a two-me

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

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

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

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

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

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

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

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

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

205 The LPS structure of B. pseudomallei, the causative agent of melioidosis, is

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

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

208 Importantly, the viability of B. pseudomallei encountered dicarbonyl toxicity was enha

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

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

211 lay a role in virulence in either the BCC or B. pseudomallei Since many of these TCS are involved in

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

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

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

215 ffect on the host response against pulmonary B. pseudomallei infection.

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

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

218 ment of in vitro and in vivo models to study B. pseudomallei gastrointestinal infection.

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

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

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

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

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

224 pithelial cells (IECs), we demonstrated that B. pseudomallei adheres, invades, and forms multinucleat

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

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

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

228 3 cells transfected with TLR5 and found that B. pseudomallei induced TLR5(1174C)- but not TLR5(1174T)

229 ion with B. pseudomallei Next, we found that B. pseudomallei-challenged TLR5-deficient (Tlr5(-/-) ) m

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

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

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

233 Overall, we showed that B. pseudomallei is an enteric pathogen and that type 1 f

234 Recent genomic studies showed that B. pseudomallei originated in Australia and spread to As

235 Finally, we also showed that B. pseudomallei requires a functional T6SS for full viru

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

237 The B. pseudomallei DeltarelA DeltaspoT mutant displayed a d

238 The B. pseudomallei flagellar protein FliC is strongly seror

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

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

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

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

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

244 ndings indicate functional redundancy of the B. pseudomallei phospholipases in virulence.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

263 physicians to provide treatment specific to B. pseudomallei In our study, we adapted host gene expre

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

265 promising antivirulence target to both treat B. pseudomallei infections and increase antibiotic effic

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

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

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

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

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

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

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

273 acking mutant MM36 compared to the wild-type B. pseudomallei strain 1026b.

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

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

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

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

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

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

280 comparable to signaling induced by virulent B. pseudomallei.

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

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

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

284 expression was up-regulated by ten-fold when B. pseudomallei was cultured under high salt concentrati

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

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

287 ected against intraperitoneal challenge with B. pseudomallei.

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

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

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

291 and hepatic compartments upon infection with B. pseudomallei Next, we found that B. pseudomallei-chal

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

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

294 develop chronic, subclinical infections with B. pseudomallei.

295 We tested blood from 33 patients with B. pseudomallei infections and 29 patients with other ba

296 eat mice infected via the aerosol route with B. pseudomallei.

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

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

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

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