ライフサイエンスコーパス: flexneri

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

2 nce of the human diarrheal pathogen Shigella flexneri.

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

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

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

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

7 la enterica serovar Typhimurium and Shigella flexneri.

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

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

10 hus compromises the invasive phenotype of S. flexneri.

11 a solani, Klebsiella pneumoniae and Shigella flexneri.

12 o study antibiotic efficacy against Shigella flexneri.

13 istant strain of the human pathogen Shigella flexneri.

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

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

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

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

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

19 BLAST search analysis revealed that the S. flexneri 2457T genome harbors 4 genes, S1242, S1289, S24

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

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

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

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

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

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

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

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

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

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

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

31 gellasonnei lineage (n = 159) and a Shigella flexneri 2a lineage (n = 105).

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

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

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

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

36 3 sites in the United States using Shigella flexneri 2a strain 2457T and Shigella sonnei strain 53G.

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 was Shigella sonnei (54.4%), followed by S. flexneri (39.2%), S. boydii (4.1%), and S. dysenteriae (

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

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

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

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

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

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

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

54 tagonists of the pathway encoded by Shigella flexneri, a cytosol-adapted bacterium, provide compellin

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

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

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

58 t the bacterial pole that is required for S. flexneri actin-based motility during intracellular infec

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

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

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

62 lonic mucosa O(2) is actively depleted by S. flexneri aerobic respiration-and not host neutrophils-du

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

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

65 S. flexneri also increases the expression of HIE proinflamm

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

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

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

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

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

71 Throughout the study period, diagnoses of S. flexneri and S. sonnei infections were most common in me

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

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

74 use of this molecular method to serotype S. flexneri and showed several advantages over the traditio

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

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

77 ax lethal toxin, Toxoplasma gondii, Shigella flexneri and the small molecule DPP8/9 inhibitor Val-bor

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

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

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

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

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

83 orthologues from Escherichia coli, Shigella flexneri, and Salmonella enterica can all fold to form s

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

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

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

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

88 Using Shigella flexneri as a model, we have previously demonstrated tha

89 Using S. flexneri as an infection model in human epithelial cells

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

91 n diarrheal disease worldwide, with Shigella flexneri being the most frequently isolated species in d

92 adhesin-like autotransporter proteins in S. flexneri biofilm formation.

93 Infection of eukaryotic cells by Shigella flexneri boosts oxygen consumption and promotes the synt

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

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

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

97 Shigella flexneri can be phenotypically serotyped using antisera

98 The bacterial pathogen Shigella flexneri causes 270 million cases of bacillary dysentery

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

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

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

102 Shigella flexneri contact with enterocytes induces a burst of pro

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

104 eamidase OspI from enteric bacteria Shigella flexneri deamidates a glutamine residue in the host ubiq

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

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

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

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

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

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

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

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

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

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

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

116 rk, we report the multiple effects of two S. flexneri effectors, IpaJ and VirA, which target small GT

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

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

119 r to humans, infant rabbits infected with S. flexneri experience severe inflammation, massive ulcerat

120 erial species, L. monocytogenes and Shigella flexneri, exploit the accessible pool of cholesterol for

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

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

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

124 A previous study showed that S. flexneri forms biofilms in the presence of bile salts, t

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

143 vivo models of shigellosis, we found that S. flexneri induces the expression of indoleamine 2,3-dioxy

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

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

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

147 prevalence was not static, with cases of S. flexneri infection in men decreasing between 2015 and 20

148 Therefore, S. flexneri infection induces a global blockage of host cel

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

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

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

152 The resolution of Shigella flexneri infection-associated hyperinflammation is cruci

153 were observed in the enteroids following S. flexneri infection.

154 sponses toward Leishmania major and Shigella flexneri infection.

155 iotic treatment significantly reduced the S. flexneri infection.

156 interacts with downstream effectors under S. flexneri infection.

157 ion from the mitochondria following Shigella flexneri infections.

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

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

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

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

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

163 agocytophilum alter host autophagy, Shigella flexneri intercepts all host pyruvate, while L. pneumoph

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

165 Shigella flexneri invades and subverts the human colonic epitheli

166 After S. flexneri invades HIE monolayers, S. flexneri replicates

167 We show that Shigella flexneri invades polarized HIE monolayers preferentially

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

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

170 disruption of HIE tight junctions enables S. flexneri invasion via the apical surface.

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

172 Shigella flexneri is a facultative intracellular organism that ca

173 Shigella flexneri is a facultative intracellular pathogen that in

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

175 Shigella flexneri is a Gram-negative intracellular pathogen that

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

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

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

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

180 Shigella flexneri is an intracellular bacterial pathogen that inv

181 Shigella flexneri is an intracellular pathogen that disseminates

182 In this study, we show that Shigella flexneri is capable of infecting and replicating intrace

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

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

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

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

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

188 Apical invasion by S. flexneri is very limited but increases ~10-fold when ent

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

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

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

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

193 In addition, the S. flexneri lux1 strain was used with an intraperitoneal (I

194 novel bioluminescent S. flexneri strain (S. flexneri lux1) was generated, which can be used in a mam

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

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

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

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

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

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

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

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

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

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

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

206 by Gram-negative pathogens such as Shigella flexneri or Salmonella Typhimurium remains incompletely

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

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

209 issemination as a critical determinant of S. flexneri pathogenesis and provides a unique small-animal

210 sporter family that is required for Shigella flexneri pathogenesis.

211 Interestingly, S. flexneri pINV also harbours two putative partitioning sy

212 In Shigella flexneri, pINV harbours three toxin-antitoxin (TA) syste

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

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

215 Shigella flexneri proliferate in infected human epithelial cells

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

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

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

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

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

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

222 After S. flexneri invades HIE monolayers, S. flexneri replicates within HIE cells and forms actin tai

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

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

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

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

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

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

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

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

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

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

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

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

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

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

237 e cytosolic Gram-negative bacterium Shigella flexneri stalls apoptosis by inhibiting effector caspase

238 A novel bioluminescent S. flexneri strain (S. flexneri lux1) was generated, which

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

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

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

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

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

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

245 S. flexneri strains containing deletion mutations in the en

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

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

248 GMMA-producing Shigella sonnei and Shigella flexneri strains.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

264 6-3770, 2011) for molecular serotyping of S. flexneri This study was performed by seven international

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

266 f NOD2 or EGFR compromises the ability of S. flexneri to induce IDO1 expression.

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

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

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

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

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

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

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

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

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

276 ation model, we identify IpaH7.8, a Shigella flexneri ubiquitin ligase secreted effector, as an enzym

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

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

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

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

281 Shigella flexneri uses its T3SS to invade human intestinal cells

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

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

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

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

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

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

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

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

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

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

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

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

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

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

296 Shigella flexneri, which replicates in the cytoplasm of intestina

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

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

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

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