ライフサイエンスコーパス: tularensis

1 to macrophage inflammation in response to F. tularensis.

2 etic pathway in macrophages infected with F. tularensis.

3 the live vaccine strain (LVS) of Francisella tularensis.

4 and the antioxidant defence mechanisms of F. tularensis.

5 ired for macrophage cytokine responses to F. tularensis.

6 l for misidentification of F. novicida as F. tularensis.

7 66c as a new virulence factor in Francisella tularensis.

8 -negative coccoid rod bacterium, Francisella tularensis.

9 establishment of a fulminate infection by F. tularensis.

10 lls with the live vaccine strain (LVS) of F. tularensis.

11 d with Dichelobacter nodosus and Francisella tularensis.

12 highly divergent sequences from Francisella tularensis.

13 the live vaccine strain (LVS) of Francisella tularensis.

14 lling survival of infection with virulent F. tularensis.

15 rucial role in innate immune responses to F. tularensis.

16 al during pulmonary infection by virulent F. tularensis.

17 ous and pulmonary infection with Francisella tularensis.

18 etween attenuated and virulent strains of F. tularensis.

19 r phagosome permeabilization by Franciscella tularensis.

20 ed resistance to pulmonary infection with F. tularensis.

21 dentified mechanism for uptake of iron by F. tularensis.

22 ring intracellular infections with type A F. tularensis.

23 by the gram-negative bacterium, Francisella tularensis.

24 mechanisms of inflammasome repression by F. tularensis.

25 sing Rift Valley fever virus and Francisella tularensis.

26 lar bears to C. burnetii, N. caninum, and F. tularensis.

27 vaccine-induced immune responses against F. tularensis.

28 role in the oxidative stress response of F. tularensis.

29 role of OxyR has not been established in F. tularensis.

30 anthracis, Yersinia pestis, and Francisella tularensis.

31 he intramacrophage growth and survival of F. tularensis.

32 acrophage growth and survival of Francisella tularensis.

33 Francisella tularensis, a Gram-negative bacterium, is the causative

34 bacterial carboxylesterase (FTT258) from F. tularensis, a homologue of human acyl protein thioestera

35 operon are the only major means by which F. tularensis acquires iron.

36 Our objective was to identify F. tularensis-activated host signaling pathways that regula

37 F. tularensis activates complement, and recent data suggest

38 ally misassembled contigs in assemblies of F.tularensis and between 31% and 100% of extensively misas

39 ) and priority pathogens such as Francisella tularensis and Burkholderia pseudomallei.

40 F. novicida is closely related to F. tularensis and exhibits high virulence in mice, but it i

41 on of host cell death during infection by F. tularensis and highlight how shifts in the magnitude and

42 enate pathway in Francisella novicida and F. tularensis and identified an unknown and previously unch

43 otential correlates of protection against F. tularensis and to expand and refine a comprehensive set

44 optical mapping data for loblolly pine and F.tularensis and used real optical mapping data for rice a

45 lasma gondii, Coxiella burnetii, Francisella tularensis, and Neospora caninum, estimate concentration

46 gnificantly, trans-translation mutants of F. tularensis are impaired in replication within macrophage

47 rrorism, but the pathogenic mechanisms of F. tularensis are largely unknown.

48 or this suppression of innate immunity by F. tularensis are not defined.

49 ns such as Coxiella burnetii and Francisella tularensis, as well as Coxiella-like and Francisella-lik

50 We found that viable Francisella tularensis, as well as Salmonella enterica bacteria tran

51 Here, we demonstrate a highly sensitive F. tularensis assay that incorporates sample processing and

52 der spectrum of growth inhibition against F. tularensis , Bacillus anthracis , and Staphylococcus aur

53 haride antigen and 31 bacteria/mL for the F. tularensis bacteria were achieved.

54 sensor formats for the detection of whole F. tularensis bacteria were developed and their performance

55 the lipopolysaccharide (LPS) of Francisella tularensis bacteria, a Tier 1 Select Agent of bioterrori

56 llus anthracis, Yersinia pestis, Francisella tularensis, Brucella spp., Burkholderia spp., and Ricket

57 llus anthracis, Yersinia pestis, Francisella tularensis, Burkholderia mallei, Burkholderia pseudomall

58 indicate that recognition of C3-opsonized F. tularensis, but not extensive cytosolic replication, pla

59 gainst infection with attenuated Francisella tularensis, but their role in infection mediated by full

60 ed and required for virulence of Francisella tularensis by subverting the host innate immune response

61 findings provide compelling evidence that F. tularensis catalase restricts reactive oxygen species to

62 Francisella tularensis causes a lethal human disease known as tulare

63 Francisella tularensis causes lethal pneumonia following infection o

64 intracellular bacterial pathogen Francisella tularensis causes tularemia, a zoonosis that can be fata

65 C 25015 and on Francisella tularensis subsp. tularensis CCUG 2112, the most virulent Francisella subs

66 c immune responses and protection against F. tularensis challenge.

67 rotective effects against virulent type A F. tularensis challenge.

68 t, we evaluated Escherichia coli-Francisella tularensis chimeric variants of tmRNA and SmpB.

69 RNA-Seq we identify those regions of the F. tularensis chromosome occupied by PmrA and those genes t

70 sociates with 252 distinct regions of the F. tularensis chromosome, but exerts regulatory effects at

71 nvolved in bacterial immune evasion, like F. tularensis clpB, can serve as a model for the rational d

72 cacy against Bacillus anthracis; Francisella tularensis; Coxiella burnetii; and Ebola, Marburg, and L

73 hepatocytic cell line compared to that of F. tularensis cultured in broth.

74 Many of these mutations render F. tularensis defective for intracellular growth.

75 ive vaccine strain) or catalase-deficient F. tularensis (DeltakatG) show distinct profiles in their H

76 The pathogenicity of F. tularensis depends on its ability to persist inside host

77 F. tularensis DNA in buffer or CFU of F. tularensis was spi

78 owever, the molecular mechanisms by which F. tularensis DsbA contributes to virulence are unknown.

79 Here, we demonstrate that F. tularensis DsbA is a bifunctional protein that oxidizes

80 ments in F. tularensis identified over 50 F. tularensis DsbA substrates, including outer membrane pro

81 , implicate the enzyme as a potential key F. tularensis effector protein, and may help elucidate a me

82 Infection with Francisella tularensis elicits innate and adaptive immune responses.

83 epresses inflammasome activation and that F. tularensis-encoded FTL_0325 mediates this effect.

84 The intracellular pathogen Francisella tularensis encodes a disulfide bond formation protein or

85 infection has led to the suggestion that F. tularensis evades detection by host innate immune survei

86 am-negative facultative anaerobe Francisella tularensis: F. tularensis subsp. tularensis (type A) and

87 Multiple independent acquisitions of F. tularensis from the environment over a short time period

88 Escape of F. tularensis from the phagosome into the cytosol of the ma

89 Francisella tularensis (Ft) is a highly infectious intracellular pat

90 such as virulent Francisella tularensis spp. tularensis (Ftt).

91 Es) with significant homology to Francisella tularensis (gamma-proteobacteria) have been characterize

92 Several in vivo screens have identified F. tularensis genes necessary for virulence.

93 identified 95 lung infectivity-associated F. tularensis genes, including those encoding the Lon and C

94 ofile of the live vaccine strain (LVS) of F. tularensis grown in the FL83B murine hepatocytic cell li

95 A REP34 knock-out strain of F. tularensis has a reduced ability to both induce encystme

96 F. tularensis has long been developed as a biological weapo

97 n both cases, forward primer for Francisella tularensis holarctica genomic DNA was surface immobilise

98 cribed as virulence-associated factors in F. tularensis Identification of these Lon substrates has th

99 Trapping experiments in F. tularensis identified over 50 F. tularensis DsbA substra

100 at targeting fixed (inactivated) Francisella tularensis (iFT) organisms to FcR in mice i.n., with MAb

101 crophages (BMDMs) to inactivated Francisella tularensis (iFt)-containing immune complexes, we observe

102 ted Listeria monocytogenes expressing the F. tularensis immunoprotective antigen IglC) as the booster

103 results also demonstrate that FTL_0325 of F. tularensis impacts proIL-1beta expression as early as 2

104 this study, we demonstrate that virulent F. tularensis impairs production of inflammatory cytokines

105 st aerosol challenge with virulent type A F. tularensis in a species other than a rodent since the or

106 Francisella tularensis in an intracellular bacterial pathogen that c

107 cartridge-based assay can rapidly detect F. tularensis in bloodstream infections directly in whole b

108 uivalents (GE) per reaction and 10 CFU/ml F. tularensis in both human and macaque blood.

109 Utilizing a mutant of F. tularensis in FTL_0325 gene, this study investigated the

110 for intracellular replication of Francisella tularensis in J774A.1 macrophages.

111 brane protein 2 localization with labeled F. tularensis in the lungs was greater in wild-type than in

112 ipid A 1-phosphatase, LpxE, from Francisella tularensis in Y. pestis yields predominantly 1-dephospho

113 reover, p38 MAPK activity is required for F. tularensis-induced COX-2 protein synthesis, but not for

114 nase 3 (JAK3) signaling are necessary for F. tularensis-induced PGE2 production.

115 Francisella tularensis induces the synthesis of prostaglandin E(2) (

116 he mechanisms that recruit neutrophils to F. tularensis-infected lungs, opsonization and phagocytosis

117 sly demonstrated that PGE(2) synthesis by F. tularensis-infected macrophages requires cytosolic phosp

118 However, in F. tularensis-infected macrophages we observed a temporal d

119 tion of AA to be converted into PGE(2) by F. tularensis-infected macrophages.

120 or memory (EM) CD4(+) T cells elicited by F. tularensis infection (postimmunization) is increased in

121 1(+) CD11b(+) cells in mice that survived F. tularensis infection also suggests a potential role for

122 Gram-negative bacterial pathogen Francisella tularensis Infection of macrophages and their subsequent

123 elucidate a mechanistic understanding of F. tularensis infection of phagocytic cells.

124 type mice highly sensitive to respiratory F. tularensis infection, and depletion beginning at 3 days

125 s dispensable for host immunity to type A F. tularensis infection, and that induced and protective im

126 literature exists on the host response to F. tularensis infection, the vast majority of work has been

127 with the extent of necrotic damage during F. tularensis infection.

128 s interleukin 12 (IL-12) protects against F. tularensis infection; this protection was lost in MIIG m

129 n of antibodies from patients with type B F. tularensis infections and that these can be used for the

130 The severe morbidity associated with F. tularensis infections is attributed to its ability to ev

131 We also report that F. tularensis inhibits ROS-dependent autophagy to promote i

132 Francisella tularensis is a bacterium replicating within the host cy

133 Francisella tularensis is a category A biodefence agent that causes

134 Francisella tularensis is a facultative bacterial pathogen that repl

135 Francisella tularensis is a facultative intracellular bacterial path

136 Francisella tularensis is a facultative intracellular bacterium that

137 Francisella tularensis is a facultative intracellular bacterium that

138 Francisella tularensis is a facultative intracellular bacterium that

139 Francisella tularensis is a facultative intracellular, Gram-negative

140 Francisella tularensis is a Gram-negative bacterium and the causativ

141 Francisella tularensis is a highly infectious bacterium that causes

142 Francisella tularensis is a highly infectious intracellular bacteriu

143 Francisella tularensis is a highly virulent Gram-negative intracellu

144 metabolic reprogramming of host cells by F. tularensis is a key component of both inhibition of host

145 Francisella tularensis is a potential bioterrorism agent that is hig

146 Although F. tularensis is a recognized biothreat agent with broad an

147 Francisella tularensis is an important human pathogen responsible fo

148 Pulmonary exposure to Francisella tularensis is associated with severe lung pathology and

149 Because of its extreme pathogenicity, F. tularensis is classified as a category A bioweapon by th

150 The adaptive immune response to Francisella tularensis is dependent on the route of inoculation.

151 Extreme infectivity and virulence of F. tularensis is due to its ability to evade immune detecti

152 f intraocular inflammation in areas where F. tularensis is endemic.

153 e in infection mediated by fully virulent F. tularensis is not known.

154 We propose that the extreme virulence of F. tularensis is partially due to the bifunctional nature o

155 The bacterium Francisella tularensis is recognized for its virulence, infectivity,

156 Such outbreaks are exceedingly rare, and F. tularensis is seldom recovered from clinical specimens.

157 Francisella tularensis is the causative agent of the debilitating fe

158 Francisella tularensis is the causative agent of tularemia and a cat

159 Francisella tularensis is the causative agent of tularemia.

160 Francisella tularensis is the etiological agent of tularemia, or rab

161 One significant virulence factor of F. tularensis is the O-polysaccharide (O-PS) portion of the

162 an essential virulence factor of Francisella tularensis, is a lipoprotein with two conserved domains

163 zoonose caused by the bacterium Francisella tularensis, largely refer to Parinaud's oculoglandular s

164 Here we establish that F. tularensis limits Ca(2+) entry in macrophages, thereby l

165 ated rabbits were seropositive for IgG to F. tularensis lipopolysaccharide (LPS).

166 larensis vs Pseudomonas aeruginosa and by F. tularensis live bacteria vs the closely related bacteriu

167 oid cells in vivo in response to Francisella tularensis Live Vaccine Strain (Ft. LVS) infection.

168 ntified TolC as a virulence factor of the F. tularensis live vaccine strain (LVS) and demonstrated th

169 Using PBLs from mice vaccinated with F. tularensis Live Vaccine Strain (LVS) and related attenua

170 e than the currently available unlicensed F. tularensis live vaccine strain (LVS) is needed to protec

171 es generated in macrophages infected with F. tularensis live vaccine strain (LVS) or the virulent Sch

172 ve now evaluated the lethality of primary F. tularensis live vaccine strain (LVS) pulmonary infection

173 Intradermal inoculation with the F. tularensis live vaccine strain (LVS) results in a robust

174 We employed Francisella tularensis live vaccine strain (LVS) to study mechanisms

175 se gene (FTL_0724) as being important for F. tularensis live vaccine strain (LVS) virulence.

176 by using unmarked deletion mutants of the F. tularensis live vaccine strain (LVS).

177 immunity against pulmonary infection with F. tularensis live vaccine strain, its production is tightl

178 mortality after pulmonary infection with F. tularensis live vaccine strain.

179 pathology during pulmonary infection with F. tularensis live vaccine strain.

180 riments identified five substrates of the F. tularensis Lon protease (FTL578, FTL663, FTL1217, FTL122

181 We were particularly interested in the F. tularensis LVS (live vaccine strain) clpB (FTL_0094) mut

182 s of MAb-iFT-immunized mice subsequent to F. tularensis LVS challenge.

183 Furthermore, F. tularensis LVS delayed pyroptotic cell death of the infe

184 monocytes and neutrophils, infected with F. tularensis LVS ex vivo, display enhanced restriction of

185 Infection of mice in vivo with a F. tularensis LVS FTL_0724 mutant resulted in diminished mo

186 infected lungs, and control of pulmonary F. tularensis LVS growth.

187 reening a transposon insertion library of F. tularensis LVS in the presence of hydrogen peroxide, we

188 Importantly, pulmonary F. tularensis LVS infection of MR1-deficient (MR1(-/-)) mic

189 We found that the lethality of pulmonary F. tularensis LVS infection was exacerbated under condition

190 ceptible than IgA(+/+) mice to intranasal F. tularensis LVS infection, despite developing higher leve

191 itical and novel regulator of immunity to F. tularensis LVS infection, its effects were masked during

192 7Ralpha(-/-) mice are more susceptible to F. tularensis LVS infection, our studies, using a virulent

193 a critical protective role in respiratory F. tularensis LVS infection.

194 4(+) T cells to the lungs after pulmonary F. tularensis LVS infection.

195 ected antigen presenting cells to control F. tularensis LVS intracellular growth.

196 presence of complement, whereas parental F. tularensis LVS is internalized within spacious pseudopod

197 growth that can be restored to wild-type F. tularensis LVS levels by either transcomplementation, in

198 These findings further illustrate that F. tularensis LVS possesses numerous genes that influence i

199 e-derived DCs (Mo-DCs) in the lungs after F. tularensis LVS pulmonary infection.

200 tively, this study provides evidence that F. tularensis LVS represses inflammasome activation and tha

201 contrast, infection of macrophages with a F. tularensis LVS rluD pseudouridine synthase (FTL_0699) mu

202 r of the oxidative stress response of the F. tularensis LVS.

203 thesized that the antioxidant defenses of F. tularensis maintain redox homeostasis in infected macrop

204 factors and the mechanisms through which F. tularensis mediates these suppressive effects remain rel

205 , we sought an alternative means by which F. tularensis might obtain iron.

206 The means by which F. tularensis modulates macrophage activation are not fully

207 revealed that the immune response to the F. tularensis mutant strains was significantly different fr

208 wth, leading us to hypothesize that these F. tularensis mutants are attenuated because they induce an

209 oli cells yielded glycOMVs that displayed F. tularensis O-PS.

210 In infected macaques, the assay detected F. tularensis on days 1 to 4 postinfection in 21%, 17%, 60%

211 remia is caused by inhalation of Francisella tularensis, one of the most infectious microbes known.

212 The data also indicate that F. tularensis pathogenesis is controlled by a highly interc

213 The Francisella tularensis pathogenicity island (FPI) encodes many prote

214 first that C1q and C3 were essential for F. tularensis phagocytosis, whereas C5 was not.

215 e demonstrate that antioxidant enzymes of F. tularensis prevent the activation of redox-sensitive MAP

216 Francisella tularensis produces a lipopolysaccharide (LPS) that is e

217 Previously, we identified seven F. tularensis proteins that induce a rapid encystment pheno

218 wherein the immunomodulatory capacity of F. tularensis relies, at least in part, on TolC-secreted ef

219 F. tularensis represses inflammasome; a cytosolic multi-pro

220 ction by the live vaccine strain (LVS) of F. tularensis Resistance is characterized by reduced lethal

221 Analysis of the MglA and SspA mutants in F. tularensis reveals that interaction between PigR and the

222 assemblies of the loblolly pine, Francisella tularensis, rice and budgerigar genomes.

223 d survival upon subsequent challenge with F. tularensis Schu S4 and provided complete protection agai

224 n blood drawn from macaques infected with F. tularensis Schu S4 at daily intervals.

225 iglE rendered Francisella tularensis subsp. tularensis Schu S4 avirulent and incapable of intracellu

226 ses (LD50) of aerosolized highly virulent F. tularensis Schu S4 had a significantly higher survival r

227 Using an F. tularensis Schu S4 mutant library, we identified strains

228 ity island genes tested are essential for F. tularensis Schu S4 virulence and further suggest that pd

229 inoculated with F. novicida U112, LVS, or F. tularensis Schu S4.

230 terminants from the select agent Francisella tularensis SCHU S4.

231 orm of the enzyme and inhibited growth of F. tularensis SchuS4 at concentrations near that of their m

232 escribe novel inhibitors against Francisella tularensis SchuS4 FabI identified from structure-based i

233 osed to virulent (Francisella tularensis ssp tularensis SchuS4).

234 tudies, using a virulent type A strain of F. tularensis (SchuS4), indicate that IL-17Ralpha(-/-) mice

235 , with MAb-iFT immune complexes, enhances F. tularensis-specific immune responses and protection agai

236 ice with the live vaccine strain (LVS) of F. tularensis, splenic IL-10 levels increased rapidly and r

237 rial pathogens, such as virulent Francisella tularensis spp. tularensis (Ftt).

238 e from mice exposed to virulent (Francisella tularensis ssp tularensis SchuS4).

239 B1a cells in defense against the virulent F. tularensis ssp. tularensis strain SchuS4.

240 ed whether complement-dependent uptake of F. tularensis strain SCHU S4 affects the survival of primar

241 cterization of Francisella tularensis subsp. tularensis strain Schu S4 mutants that lack functional i

242 strate that lipids enriched from virulent F. tularensis strain SchuS4, but not attenuated live vaccin

243 ense against the virulent F. tularensis ssp. tularensis strain SchuS4.

244 e infected with the prototypical virulent F. tularensis strain, Schu S4.

245 erosolized Francisella tularensis subspecies tularensis, strain SCHU S4.

246 nt clues for further understanding of the F. tularensis stress response and pathogenesis.

247 tion against challenge with two different F. tularensis subsp. holarctica (type B) live vaccine strai

248 tularensis subsp. tularensis (type A) and F. tularensis subsp. holarctica (type B).

249 de putative TPR-like proteins in Francisella tularensis subsp. holarctica FSC200.

250 ereby contributing to the survival of the F. tularensis subsp. holarctica live vaccine strain (LVS) i

251 DI-TOF) mass spectrometry on the Francisella tularensis subsp. holarctica LVS defined three protein b

252 ultative anaerobe Francisella tularensis: F. tularensis subsp. tularensis (type A) and F. tularensis

253 cluster from the highly virulent Francisella tularensis subsp. tularensis (type A) strain Schu S4 in

254 a philomiragia ATCC 25015 and on Francisella tularensis subsp. tularensis CCUG 2112, the most virulen

255 of both copies of iglE rendered Francisella tularensis subsp. tularensis Schu S4 avirulent and incap

256 solation and characterization of Francisella tularensis subsp. tularensis strain Schu S4 mutants that

257 F. tularensis subspecies holarctica was isolated from the b

258 masome during infection with the Francisella tularensis subspecies novicida (F. novicida), whereas en

259 During F. tularensis subspecies novicida infection, AIM2, an infla

260 e to lethal doses of aerosolized Francisella tularensis subspecies tularensis, strain SCHU S4.

261 level with the identification of Francisella tularensis subspecies.

262 n of endogenous protein-tagging events in F. tularensis that are likely to be a universal feature of

263 outbreak was caused by diverse clones of F. tularensis that occurred concomitantly, were widespread,

264 ts close genetic relationship to Francisella tularensis, the agent of tularemia.

265 Francisella tularensis, the bacterial cause of tularemia, infects th

266 Francisella tularensis, the causative agent of a fatal human disease

267 Francisella tularensis, the causative agent of tularemia, is a categ

268 Francisella tularensis, the causative agent of tularemia, is a highl

269 Francisella tularensis, the causative agent of tularemia, is most de

270 Francisella tularensis, the causative agent of tularemia, is one of

271 Francisella tularensis, the causative agent of tularemia, modulates

272 Francisella tularensis, the etiological agent of tularemia, is one o

273 gainst intentional release of aerosolized F. tularensis, the most dangerous type of exposure.

274 In Francisella tularensis, the putative DNA-binding protein PigR works

275 anism of immune evasion is the ability of F. tularensis to induce the synthesis of the small lipid me

276 ls novel pathogenic mechanisms adopted by F. tularensis to modulate macrophage innate immune function

277 delay in host cell death is required for F. tularensis to preserve its intracellular replicative nic

278 nse mechanisms, as well as the ability of F. tularensis to prolong neutrophil lifespan.

279 Based on the ability of F. tularensis to resist high ROS/RNS levels, we have hypoth

280 er, the factors that govern adaptation of F. tularensis to the intrahepatocytic niche have not been i

281 as the highly virulent bacterium Francisella tularensis, to ensure their replication and transmission

282 d that lon and clpP are also required for F. tularensis tolerance to stressful conditions.

283 on the highly virulent bacterium Francisella tularensis tularensis.

284 e against attenuated F. tularensis versus F. tularensis type A differs.

285 FTT_0166c in the highly virulent Francisella tularensis type A strain SchuS4 are required for proper

286 of mice infected with the LVS rather than F. tularensis type A, while IL-23p19 mRNA expression was fo

287 Francisella tularensis: F. tularensis subsp. tularensis (type A) and F. tularensis subsp. holarctica

288 ighly virulent Francisella tularensis subsp. tularensis (type A) strain Schu S4 in hypervesiculating

289 ccine-induced protection against Francisella tularensis using murine splenocytes and further demonstr

290 The Gram-negative bacterium Francisella tularensis utilizes its antioxidant armature to limit th

291 ective immune response against attenuated F. tularensis versus F. tularensis type A differs.

292 A hallmark of F. tularensis virulence is its ability to quickly grow to h

293 F. tularensis virulence stems from genes encoded on the Fra

294 1548 and FTL_1709, which are required for F. tularensis virulence.

295 n to modulate both isomerase activity and F. tularensis virulence.

296 Thus, IglE is essential for Francisella tularensis virulence.

297 nal transducer and model drug by LPS from F. tularensis vs Pseudomonas aeruginosa and by F. tularensi

298 as early as 4 hrs post-exposure, Francisella tularensis was associated with an almost complete lack o

299 F. tularensis DNA in buffer or CFU of F. tularensis was spiked into human or macaque blood.

300 Only the OxyR homolog is present in F. tularensis, while the SoxR homologs are absent.