ライフサイエンスコーパス: flexneri

1 almonella enterica SPI-2), or MxiH (Shigella flexneri).

2 d-type intracellular growth and spread of S. flexneri.

3 its regulation by H-NS and VirB in Shigella flexneri.

4 during invasion and that are specific to S. flexneri.

5 d for IcsA secretion at the pole in Shigella flexneri.

6 A. hydrophila and the vacB gene of Shigella flexneri.

7 hus compromises the invasive phenotype of S. flexneri.

8 IcsA localization and plaque formation by S. flexneri.

9 not interchangeable in S. typhimurium and S. flexneri.

10 that of T84 cells infected with wild-type S. flexneri.

11 confluent monolayers similar to wild-type S. flexneri.

12 both of these systems were constructed in S. flexneri.

13 istant strain of the human pathogen Shigella flexneri.

14 iological effects of iron availability in S. flexneri.

15 infection by the T3SS-dependent pathogen S. flexneri.

16 ous process over time with GFP-expressing S. flexneri.

17 nce of the human diarrheal pathogen Shigella flexneri.

18 that it is not critical for intracellular S. flexneri.

19 ri 6, S. flexneri 3a, S. flexneri 2b, and S. flexneri 1b.

20 he Enterobacteriaceae Characterization of S. flexneri 2457T biofilms determined that both bile salts

21 Our data demonstrate that S. flexneri 2457T employs multiple mechanisms to survive ex

22 portant physiological signals to activate S. flexneri 2457T virulence.

23 tant bile salt transcriptional profile in S. flexneri 2457T, including induced drug resistance and vi

24 The commonest serotype was Shigella flexneri 2a (89 of 292 serotypes [30.5%]).

25 dominantly hexaacylated lipid A) or Shigella flexneri 2a (a mixture of hexaacylated, pentaacylated, a

26 antly, mice prevaccinated with attenuated S. flexneri 2a (SC602) strain were protected against intrap

27 , intraperitoneal challenge with virulent S. flexneri 2a (YSH6000) resulted in diarrhea and severe bo

28 t intraperitoneal challenge with virulent S. flexneri 2a can provoke bacillary dysentery and severe p

29 Of note, virulent S. flexneri 2a could invade and colonize not only systemic

30 erica serovar Typhi CVD 908-htrA or Shigella flexneri 2a CVD 1208S live vector and were boosted paren

31 yltransferases, were deleted in the Shigella flexneri 2a human challenge strain 2457T to evaluate the

32 We determine that OmpA of Shigella flexneri 2a is recognized by TLR2 and consequently media

33 This S flexneri 2a lineage is a well adapted pathogen that has

34 Genomic islands gained in the S flexneri 2a lineage over time were predominately associa

35 stent with a reduced endotoxic potential, S. flexneri 2a msbB mutants were attenuated in an acute mou

36 These results demonstrate that S. flexneri 2a OmpA may play a critical role in the develop

37 ty was significantly lower in response to S. flexneri 2a than E. coli LPS and further decreased in po

38 deletion mutations in the guaBA operon in S. flexneri 2a vaccine strains in clinical studies, we deve

39 om the O-specific polysaccharide of Shigella flexneri 2a, a major cause of bacillary dysentery.

40 and uropathogenic Escherichia coli, Shigella flexneri 2a, and the hybrid enteroaggregative/Shiga toxi

41 t vaccine with O antigens from S. sonnei, S. flexneri 2a, S. flexneri 3a, and S. flexneri 6 can provi

42 comprised 89.4% of S. flexneri, including S. flexneri 2a, S. flexneri 6, S. flexneri 3a, S. flexneri

43 a class 2 SPATE protein produced by Shigella flexneri 2a, uropathogenic and enteroaggregative Escheri

44 exneri 2a, S. flexneri 6, S. flexneri 3a, S. flexneri 2b, and S. flexneri 1b.

45 ole, and tetracycline, including 49 Shigella flexneri (33%) and 3 Shigella sonnei (0.3%) isolates.

46 e identified a recently emerged lineage of S flexneri 3a that has spread intercontinentally in less t

47 antigens from S. sonnei, S. flexneri 2a, S. flexneri 3a, and S. flexneri 6 can provide broad direct

48 including S. flexneri 2a, S. flexneri 6, S. flexneri 3a, S. flexneri 2b, and S. flexneri 1b.

49 nnei, S. flexneri 2a, S. flexneri 3a, and S. flexneri 6 can provide broad direct coverage against the

50 ed for the NleE homologue OspZ from Shigella flexneri 6 that also bound TAB3 through the (49)GITR(52)

51 of S. flexneri, including S. flexneri 2a, S. flexneri 6, S. flexneri 3a, S. flexneri 2b, and S. flexn

52 Shigella flexneri, a causative agent of bacterial dysentery, poss

53 Shigella flexneri, a gram-negative enteric pathogen, is unusual i

54 However, Shigella flexneri, a nonflagellated bacterium, and a flagellin (f

55 transcriptional immune response to Shigella flexneri across different infection stages in bulk and s

56 S. flexneri actin-based motility has been characterized in

57 Here we characterized S. flexneri actin-based motility in HT-29 intestinal cells.

58 that S. enterica serovar Typhimurium and S. flexneri activate different subtypes of phospholipase A(

59 thogens, including IcsA and SepA of Shigella flexneri, AIDA-I of diffusely adherent Escherichia coli,

60 Interestingly, the wild-type S. flexneri also formed larger plaques in the presence of s

61 In HeLa229 cells, S. flexneri also formed membrane protrusions that extended

62 eedle protein through the needle of Shigella flexneri, an essential step during needle assembly, we h

63 protective efficacy was 70% against Shigella flexneri and 50% against Shigella sonnei.

64 anism in enteroinvasive E. coli and Shigella flexneri and as a factor mediating E. coli O157:H7 adher

65 Intracellular pathogens such as Shigella flexneri and Listeria monocytogenes achieve disseminatio

66 icient T3SS translocation of effectors by S. flexneri and other pathogens that use T3SS, Salmonella e

67 gues in pathogenic bacteria such as Shigella flexneri and Pseudomonas aeruginosa.

68 the ability to protect mice against Shigella flexneri and S. sonnei in the lethal pulmonary challenge

69 cause of bacterial dysentery, with Shigella flexneri and Shigella sonnei accounting for around 90% o

70 nst lethal pulmonary infection with Shigella flexneri and Shigella sonnei.

71 ithin the N-terminal regions of IpaB from S. flexneri and SipB from Salmonella enterica serovar Typhi

72 ponse to low iron concentrations in Shigella flexneri and that this occurs at the level of transcript

73 ytoplasmic regions of the vT3SSs of Shigella flexneri and the vT3SS and fT3SS of Salmonella enterica

74 la enterica serovar Typhimurium and Shigella flexneri and to the formation of attaching and effacing

75 o evaluate a real-time PCR for serotyping S. flexneri and to use whole-genome sequencing (WGS) to inv

76 ichia coli, Salmonella typhimurium, Shigella flexneri, and Burkholderia thailandensis activates mouse

77 enteropathogenic Escherichia coli, Shigella flexneri, and Campylobacter jejuni, but not Neisseria go

78 Since Listeria monocytogenes, Shigella flexneri, and Vaccinia virus among other pathogens use t

79 o investigate if HeLa cells infected with S. flexneri are able to resist the induction of apoptosis f

80 nd the psp genes of S. enterica and Shigella flexneri are highly induced during macrophage infection.

81 hogenic Escherichia coli (EPEC) and Shigella flexneri are human host-specific pathogens that infect i

82 entium, Salmonella typhimurium, and Shigella flexneri are sensed in an ill-defined manner by an intra

83 ithelial Caco-2 cell monolayers and Shigella flexneri as a model enteropathogen, we found that polysp

84 ram-negative bacterium Shigella flexneri (S. flexneri) as a first step of bacteriophage infection.

85 gainst the enteroinvasive bacterium Shigella flexneri, both in vitro and in vivo.

86 he movement of the enteric pathogen Shigella flexneri, both within the cell body and from cell to cel

87 in stability and is present in pINV from S. flexneri but absent in S. sonnei pINV.

88 spF and OspC1 are known to be secreted by S. flexneri, but their functions are unknown.

89 Shigella flexneri can be phenotypically serotyped using antisera

90 Shigella flexneri causes a severe form of bacillary dysentery als

91 Shigella flexneri causes dysentery after invading the epithelial

92 Shigella flexneri causes human dysentery after invading the cells

93 Although S. flexneri causes most disease in low-income countries (fo

94 S. enterica serovar Typhimurium and S. flexneri cell entry was dependent on the Salmonella path

95 ectively, of 1130 Shigella case isolates; S. flexneri comprised 65.9% and S. sonnei 23.7%.

96 Shigella flexneri contact with enterocytes induces a burst of pro

97 e large virulence plasmid pWR100 of Shigella flexneri contains a new P1par family member: pWR100par.

98 The tip complex of Shigella flexneri contains invasion plasmid antigen D (IpaD), whi

99 A Shigella flexneri degP mutant, which was defective for plaque for

100 In contrast, in the S. flexneri DeltahtrB mutant, a compensatory lipid A palmit

101 tions relative to the epithelial surface, S. flexneri density within the tissue, and volume of tissue

102 ent and invasion by deoxycholate in Shigella flexneri, deoxycholate negatively regulates IcsA and MAM

103 ve immunity to the enteric pathogen Shigella flexneri, despite the ability of Shigella to actively se

104 ion profiles of wild type and dksA mutant S. flexneri determined that hfq expression was reduced in t

105 We found that although S. flexneri displayed comparable actin-based motilities in

106 nt for tyrosine kinase signaling promotes S. flexneri dissemination in epithelial cells.

107 S. flexneri dissemination in HT-29 cells led to the local p

108 We suggest a model of S. flexneri dissemination in which the formation of VLPs is

109 dylinositol 3-phosphate kinase PIK3C2A in S. flexneri dissemination.

110 ndidate interaction partners of the Shigella flexneri effector proteins OspE1 and OspE2, which contai

111 , the professional cytosol-dwelling Shigella flexneri escapes from LUBAC-mediated restriction through

112 onnei plasmid is less stable than that of S. flexneri, especially at environmental temperatures.

113 ofluorescence of HeLa cells infected with S. flexneri expressing OspF-2HA or OspC1-2HA revealed that

114 ntribute to immune evasion of E. coli and S. flexneri, favoring invasiveness and increasing the sever

115 either E. coli or V. cholerae Feo, or the S. flexneri ferrous iron transport system Sit, restored Vci

116 irmed the bias of experimentally measured S. flexneri for early crypt targeting.

117 e that the acid sensitivity defect of the S. flexneri fur mutant is due to repression of ydeP by RyhB

118 plete media, and addition of either Shigella flexneri fur or Sodalis fur to a plasmid restored normal

119 oarray analysis was performed to identify S. flexneri genes differentially regulated by the NtrBC sys

120 are) remaining subserotype through shared S. flexneri group antigens.

121 with three distinct growth environments: S. flexneri growing in broth (in vitro), S. flexneri growin

122 S. flexneri growing in broth (in vitro), S. flexneri growing within epithelial cell cytoplasm (intra

123 genes provide a competitive advantage to S. flexneri growing within epithelial cells, and a sitA mut

124 ly uncharacterized for potential roles in S. flexneri growth within the eukaryotic intracellular envi

125 ing that Listeria monocytogenes and Shigella flexneri have evolved pathogen-specific mechanisms of ba

126 normal production and localization of the S. flexneri IcsA protein.

127 rsinia pestis YapV is homologous to Shigella flexneri IcsA, and like IcsA, YapV recruits mammalian ne

128 ylate-binding proteins (GBPs) coats Shigella flexneri in a hierarchical manner reliant on GBP1.

129 protocol was devised to follow individual S. flexneri in a large tissue volume.

130 of the Vps/VacJ ABC transporter system in S. flexneri in both the maintenance of lipid asymmetry in t

131 and contributes to cell-to-cell spread of S. flexneri in cell culture.

132 Pyruvate increased the growth rate of S. flexneri in vitro, suggesting that it may be a preferred

133 dies with three omp null mutants of Shigella flexneri, including classic phage plaque assays and time

134 invasion and cell-to-cell spread by Shigella flexneri, including multiple components of the type thre

135 serotypes/subserotypes comprised 89.4% of S. flexneri, including S. flexneri 2a, S. flexneri 6, S. fl

136 Characterization of the sitABCD genes in S. flexneri indicates that they encode a ferrous iron trans

137 Here we uncover a mechanism for Shigella flexneri-induced actin comet tail elongation that links

138 ific CD8(+) T cells are not primed during S. flexneri infection and, as a result, afford little prote

139 ependence on the activation of Dia during S. flexneri infection contrasts with the inhibition of this

140 information regarding the progression of S. flexneri infection in an unbiased and exhaustive manner.

141 demonstrate that activation of PKC during S. flexneri infection is attenuated in the absence of PDLIM

142 esponse to infection, which suggests that S. flexneri infection not only triggers the production of p

143 teropathogenic Escherichia coli and Shigella flexneri infection, WASp deficiency causes defective bac

144 ion from the mitochondria following Shigella flexneri infections.

145 We previously demonstrated that S. flexneri inhibits staurosporine-induced apoptosis in inf

146 u structures of the Y. enterocolitica and S. flexneri injectisomes had similar dimensions and were si

147 ture of Yersinia enterocolitica and Shigella flexneri injectisomes in situ and the first structural a

148 Signals resulting from S. flexneri interactions with subcapsular sinus macrophages

149 fection of human colonic tissue, invasive S. flexneri interacts with and occasionally invades B lymph

150 ted and is short-lasting, suggesting that S. flexneri interferes with the priming of specific immunit

151 In contrast, S. flexneri invades the large intestine epithelium at the b

152 gluconeogenic pathways influence steps in S. flexneri invasion and plaque formation.

153 The guinea pig model for Shigella flexneri invasion of the colonic mucosa was used to moni

154 dioactive iron by the Feo system into the S. flexneri iron transport mutant was stimulated by the red

155 Shigella flexneri is a bacterial pathogen that invades cells of t

156 Shigella flexneri is a facultative intracellular organism that ca

157 Shigella flexneri is a facultative intracellular pathogen that ca

158 Shigella flexneri is a facultative intracellular pathogen that in

159 Shigella flexneri is a Gram-negative enteric pathogen that is the

160 Shigella flexneri is a Gram-negative intracellular pathogen that

161 Shigella flexneri is a Gram-negative pathogen that invades the co

162 Shigella flexneri is a gram-negative, facultative intracellular p

163 The LPS of the enteropathogen Shigella flexneri is a hexa-acylated isoform possessing an optima

164 utative NF-T3SS C-ring component in Shigella flexneri is alternatively translated to produce both ful

165 Shigella flexneri is an enteropathogen responsible for severe dys

166 Shigella flexneri is an intracellular pathogen that disseminates

167 The active needle tip complex of S. flexneri is composed of a tip protein, IpaD, and two por

168 type-III secretion system needle of Shigella flexneri is determined to a precision of 0.4 A.

169 e of the large virulence plasmid of Shigella flexneri is highly dependent on one of its PSK systems,

170 ion of epithelial cells from apoptosis by S. flexneri is regulated by one or more of the bacterial ge

171 m-negative enteroinvasive bacterium Shigella flexneri is responsible for the endemic form of bacillar

172 Shigella flexneri is the causative agent of dysentery, and its pa

173 important function of GBP recruitment to S. flexneri is to prevent the spread of infection to neighb

174 reference genome of the historical Shigella flexneri isolate NCTC1 and to examine the isolate for re

175 yses identified genes that are present in S. flexneri isolates but not in the three other Shigella sp

176 i or S. boydii by the kmer ID, and 8 were S. flexneri isolates misidentified by TB&S as S. boydii due

177 We believe that S. flexneri, like other pathogens, inhibits apoptosis in ep

178 by which each of the two MsbB proteins of S. flexneri likely contributes to pathogenesis.

179 at the type III effector IpgB1 from Shigella flexneri may bind to acidic phospholipids and regulate a

180 In order to thrive in the host, S. flexneri must adapt to environmental conditions in the g

181 coli and also conferred growth on a Shigella flexneri mutant that has a severe defect in iron transpo

182 in both rich and minimal media of a Shigella flexneri mutant that produces no siderophores.

183 Analysis of S. flexneri mutants showed that invasion and a functional t

184 f these pathways is used by intracellular S. flexneri, mutants were constructed and tested in a plaqu

185 s family, the crystal structures of Shigella flexneri MxiC we present here confirm the conservation o

186 rmined the crystal structure of the Shigella flexneri MxiH needle.

187 , Escherichia coli (EprJ and EscI), Shigella flexneri (MxiI), and Pseudomonas aeruginosa (PscI).

188 has previously been shown that the Shigella flexneri needle has a helical symmetry of approximately

189 previously that the monomer of the Shigella flexneri needle, MxiH, assembles into a helical structur

190 by TB&S as S. boydii due to nonfunctional S. flexneri O antigen biosynthesis genes.

191 e immunity, we investigated the impact of S. flexneri on T-cell dynamics in vivo.

192 e, MD) for confirmation and serotyping of S. flexneri; one-third of isolates were sent to the Centers

193 isolates that were misidentified as Shigella flexneri or S. boydii by the kmer ID, and 8 were S. flex

194 exploit two effector proteins, the Shigella flexneri OspF protein and Yersinia pestis YopH protein,

195 H2), display sequence similarity to Shigella flexneri OspG, which inhibits activation of the pro-infl

196 The invasin IpaA is essential for S. flexneri pathogenesis and binds to the cytoskeletal prot

197 sporter family that is required for Shigella flexneri pathogenesis.

198 bmucosa, which are fundamental aspects of S. flexneri pathogenesis.

199 f IroE to the structure of Fes from Shigella flexneri (PDB entry 2B20).

200 Escherichia coli strains expressing Shigella flexneri plasmid and chromosomal virulence factors for e

201 cific parameters included the analysis of S. flexneri positions relative to the epithelial surface, S

202 Shigella flexneri possesses at least two putative high-affinity m

203 Shigella flexneri proliferate in infected human epithelial cells

204 utotransporter secreted by EAEC and Shigella flexneri, promote colonization of the mouse.

205 HK97, S. enterica phage ST64T, or a Shigella flexneri prophage.

206 Recently, the Shigella flexneri protease IpaJ was found to cleave myristoylated

207 PIK3C2A-mediated PtdIns(3)P production in S. flexneri protrusions was regulated by host cell tyrosine

208 An S. flexneri pst mutant forms smaller plaques in Henle cell

209 This suggested that the inability of the S. flexneri pst mutant to form wild-type plaques in Henle c

210 e, and undertook comparative genetics with S flexneri reference strains isolated during the 100 years

211 ted in various cell lines, we showed that S. flexneri relies on neural Wiskott-Aldrich Syndrome prote

212 Both EPEC and S. flexneri rely on type three secretion systems (T3SS) to

213 The pathogenesis of Shigella flexneri requires a functional type III secretion appara

214 Shigella flexneri requires iron for survival, and the genes for i

215 Mutations in vps or vacJ in Shigella flexneri resulted in increased sensitivity to lysis by t

216 ial cells with an ospZ deletion mutant of S. flexneri resulted in reduced PMN transepithelial migrati

217 ride of the Gram-negative bacterium Shigella flexneri (S. flexneri) as a first step of bacteriophage

218 ers of each of the four Shigella species: S. flexneri, S. sonnei, S. boydii, and S. dysenteriae.

219 S. flexneri secretes effector proteins into the eukaryotic

220 sis, we sequenced the oldest extant Shigella flexneri serotype 2a isolate using single-molecule real-

221 nome sequenced clinical isolates of Shigella flexneri serotype 3a from high-risk and low-risk regions

222 We obtained 331 clinical isolates of S flexneri serotype 3a, including 275 from low-risk region

223 ine must protect against S. sonnei and 15 S. flexneri serotypes/subserotypes.

224 ) and its homolog YggD protein from Shigella flexneri (Sf-YggD).

225 in E.coli EDL933, E.coli CFT073 and Shigella flexneri Sf301.

226 that S. enterica serovar Typhimurium and S. flexneri share certain elements in the mechanism(s) that

227 coli strain CFT073, homologs of the Shigella flexneri SHI-2 pathogenicity island gene shiA, suppress

228 Studies with Shigella flexneri show that hfq transcription is regulated by a p

229 Expression of the S. flexneri sit and mntH promoters was higher when Shigella

230 The Shigella flexneri sit genes can be lost as a result of deletion w

231 S. flexneri skp and surA mutants failed to form plaques in

232 nd 2.8 A and a wild-type PCP-1 from Shigella flexneri solved at 2.8 A.

233 Shigella flexneri Spa15 is a chaperone of the type 3 secretion sy

234 h highlighting induced virulence in Shigella flexneri strain 2457T following exposure to bile salts.

235 oteomic analysis was performed with Shigella flexneri strain 2457T in association with three distinct

236 To test our hypothesis, S. flexneri strain 2457T was subcultured in media containin

237 when vciB was expressed in an E. coli or S. flexneri strain defective for the ferrous iron transport

238 alize intact machines in a virulent Shigella flexneri strain genetically modified to produce minicell

239 fic CD8(+) T-cell response, we created an S. flexneri strain that constitutively secretes a viral CD8

240 S. flexneri strains containing deletion mutations in the en

241 r growth stimulation of E. coli and Shigella flexneri strains in low-iron medium.

242 They characterized tgt- mutant S. flexneri strains in which the translation of VirF is mar

243 GMMA-producing Shigella sonnei and Shigella flexneri strains.

244 The human pathogen Shigella flexneri subverts host function and defenses by deployin

245 Expression from the S. flexneri suf and isc promoters increased when Shigella w

246 IpaC is then transported to the S. flexneri surface when target cell lipids are added, and

247 tion induction or IpaC recruitment to the S. flexneri surface.

248 iscovered that Orf212 was secreted by the S. flexneri T3SS and renamed this protein OspZ.

249 port that OspB can be added to the set of S. flexneri T3SS effectors required to modulate the innate

250 These findings indicate that S. flexneri targets T lymphocytes in vivo and highlight the

251 Escherichia coli TGT (99% identity to the S. flexneri TGT) in vitro.

252 wer (approximately 20-90%) in response to S. flexneri than to E. coli LPS/lipid A and PBMC from polym

253 an essential virulence function for Shigella flexneri that delivers effector proteins that are respon

254 ecretion system (T3SS) effectors of Shigella flexneri that downregulate the host innate immune respon

255 elial cell cytoplasm (intracellular), and S. flexneri that were cultured with, but did not invade, He

256 other enteric pathogens, including Shigella flexneri, that express similar proteins.

257 ecreted in response to infection by Shigella flexneri, that it is produced by a pathway involving 12/

258 Shigella flexneri, the causative agent of bacillary dysentery, in

259 Here, we show that infection by Shigella flexneri, the causative agent of human bacillary dysente

260 Shigella flexneri, the causative agent of shigellosis, is a gram-

261 Sf6, a P22-like phage that infects Shigella flexneri, the tail needle presents a C-terminal globular

262 n, but are required for stable docking of S. flexneri to cells; moreover, stable docking triggers eff

263 P or PoxA leads to an impaired ability of S. flexneri to invade epithelial cells and form plaques in

264 rbon metabolism may be key factors in the S. flexneri transition from the extra- to the intracellular

265 Shigella flexneri two-component regulatory systems (TCRS) are res

266 nas aeruginosa covalently linked to Shigella flexneri type 2a O-antigen (Sf2E) produced by engineered

267 naling and relied on the integrity of the S. flexneri type 3 secretion system (T3SS).

268 IpaJ), a previously uncharacterized Shigella flexneri type III effector protein with cysteine proteas

269 Thus, the S. flexneri type III secretion system can be induced in a s

270 he identification of two homologous Shigella flexneri type III secretion system effector E3 ligases I

271 -glucosylation patterns encountered among S. flexneri type-specific polysaccharides.

272 el increased bacterial clearance of Shigella flexneri upon colonic infection, strongly suggesting tha

273 ma-derived IgA and SIgA neutralized Shigella flexneri used as a model pathogen, resulting in a delay

274 S. flexneri uses a type III secretion system to inject effe

275 The pathogenic bacterium Shigella flexneri uses a type III secretion system to inject viru

276 Shigella flexneri uses its T3SS to invade human intestinal cells

277 Shigella flexneri uses its type III secretion apparatus (TTSA) to

278 Shigella flexneri uses its type III secretion system (T3SS) to pr

279 hough S. enterica serovar Typhimurium and S. flexneri utilize different mechanisms for triggering the

280 IpaA subverts vinculin's functions, where S. flexneri utilizes a remarkable level of molecular mimicr

281 ty is initiated, we provide evidence that S. flexneri, via its type III secretion system, impairs the

282 ts was due to decreased expression of the S. flexneri virulence factor regulators virF and virB, resu

283 The expression of a subset of Shigella flexneri virulence genes is dependent upon a cytoplasmic

284 s CsrA and Cra in a cell culture model of S. flexneri virulence.

285 sion and this regulation is important for S. flexneri virulence.

286 l migration in response to infection with S. flexneri was dependent on 12/15-LOX activity, the enzyme

287 octamers, whereas the wild-type WzzB from S. flexneri was found to be an open trimer.

288 ing bacteriophage Sf6 and its host, Shigella flexneri, we investigated how Sf6 utilizes outer membran

289 il to play a role in adaptive immunity to S. flexneri, we investigated whether antigen-specific CD8(+

290 both S. enterica serovar Typhimurium and S. flexneri were located in intracellular niches in ES cell

291 ogenetic relationships between strains of S. flexneri WGS data provided both genome-derived serotypin

292 r efficient entry and cell-cell spread of S. flexneri, whereas the lower affinity VBS appears to cont

293 Here we show that Shigella flexneri, which causes dysentery, encounters varying oxy

294 Shigella flexneri, which replicates in the cytoplasm of intestina

295 We transformed S. flexneri with a plasmid that expresses a two-hemagglutin

296 points, there was a clear association of S. flexneri with crypts, key morphological features of the

297 red that NCTC1 belonged to a 2a lineage of S flexneri, with which it shares common characteristics an

298 emagglutinin-tagged spa15 was secreted by S. flexneri within 2 h in the Congo red secretion assay, an

299 samples further confirmed the location of S. flexneri within colonocytes at the mouth of crypts.

300 Furthermore, an S. flexneri ydeP mutant was defective for both glutamate-in