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1                                              S. flexneri actin-based motility has been characterized
2                                              S. flexneri also increases the expression of HIE proinfl
3                                              S. flexneri dissemination in HT-29 cells led to the loca
4                                              S. flexneri mutants that contain a disruption in the cyd
5                                              S. flexneri secretes effector proteins into the eukaryot
6                                              S. flexneri skp and surA mutants failed to form plaques
7                                              S. flexneri strains containing deletion mutations in the
8                                              S. flexneri uses a type III secretion system to inject e
9                                              S. flexneri-infected cells were used as a control.
10 accine must protect against S. sonnei and 15 S. flexneri serotypes/subserotypes.
11  cryptic prophages, 372 pseudogenes, and 195 S. flexneri-specific genes.
12            Disruption of icsP in serotype 2a S. flexneri leads to a marked reduction in IcsA cleavage
13 ctin-based motility of wild-type serotype 2a S. flexneri.
14 h O antigens from S. sonnei, S. flexneri 2a, S. flexneri 3a, and S. flexneri 6 can provide broad dire
15 4% of S. flexneri, including S. flexneri 2a, S. flexneri 6, S. flexneri 3a, S. flexneri 2b, and S. fl
16  flexneri 2a, S. flexneri 6, S. flexneri 3a, S. flexneri 2b, and S. flexneri 1b.
17 ri, including S. flexneri 2a, S. flexneri 6, S. flexneri 3a, S. flexneri 2b, and S. flexneri 1b.
18 report represents the first description of a S. flexneri gene identified based on enhanced expression
19   Addition of this pstA(R220Q) mutation to a S. flexneri pst mutant, as part of the pst operon, resto
20  important physiological signals to activate S. flexneri 2457T virulence.
21                  We identified an additional S. flexneri putative iron transport gene, sitA, in a scr
22                                        After S. flexneri invades HIE monolayers, S. flexneri replicat
23 linked immunosorbent assay responses against S. flexneri 2a lipopolysaccharide in two-thirds of the v
24 2-hybridizing sequences were detected in all S. flexneri strains tested and parts of the island were
25                                     Although S. flexneri causes most disease in low-income countries
26                       We found that although S. flexneri displayed comparable actin-based motilities
27 f O-glucosylation patterns encountered among S. flexneri type-specific polysaccharides.
28                                           An S. flexneri pst mutant forms smaller plaques in Henle ce
29 ecific CD8(+) T-cell response, we created an S. flexneri strain that constitutively secretes a viral
30                              Furthermore, an S. flexneri ydeP mutant was defective for both glutamate
31                                  However, an S. flexneri rpoS mutant formed plaques on tissue culture
32 xneri 6, S. flexneri 3a, S. flexneri 2b, and S. flexneri 1b.
33  sonnei, S. flexneri 2a, S. flexneri 3a, and S. flexneri 6 can provide broad direct coverage against
34 th shared and unique epitopes on E. coli and S. flexneri type 1 fimbriae.
35  contribute to immune evasion of E. coli and S. flexneri, favoring invasiveness and increasing the se
36 eltaguaB-A DeltavirG Deltaset1 Deltasen) and S. flexneri 3a strain CVD 1211 (DeltaguaB-A DeltavirG De
37 situ structures of the Y. enterocolitica and S. flexneri injectisomes had similar dimensions and were
38                                Both EPEC and S. flexneri rely on type three secretion systems (T3SS)
39 ithelial cell cytoplasm (intracellular), and S. flexneri that were cultured with, but did not invade,
40 roys these cells, while L. monocytogenes and S. flexneri appear to be internalized into M cells in a
41           Since attenuated serovar Typhi and S. flexneri can deliver measles DNA vaccines mucosally i
42 und that S. enterica serovar Typhimurium and S. flexneri activate different subtypes of phospholipase
43          S. enterica serovar Typhimurium and S. flexneri cell entry was dependent on the Salmonella p
44 and that S. enterica serovar Typhimurium and S. flexneri share certain elements in the mechanism(s) t
45 although S. enterica serovar Typhimurium and S. flexneri utilize different mechanisms for triggering
46 hat both S. enterica serovar Typhimurium and S. flexneri were located in intracellular niches in ES c
47 re not interchangeable in S. typhimurium and S. flexneri.
48 ed mucosal IgA (in tears) and serum IgG anti-S. flexneri 2a O antibodies.
49 nterrupted in the same open reading frame as S. flexneri ispA.
50  SC602 is the first example of an attenuated S. flexneri 2a candidate vaccine that provides protectio
51 ortantly, mice prevaccinated with attenuated S. flexneri 2a (SC602) strain were protected against int
52                       A novel bioluminescent S. flexneri strain (S. flexneri lux1) was generated, whi
53 mmon origin for the aerobactin genes in both S. flexneri and E. coli pColV.
54 is shown here that clinical isolates of both S. flexneri and Shigella sonnei invade epithelial cells
55 ection of epithelial cells from apoptosis by S. flexneri is regulated by one or more of the bacterial
56  colonic mucosa O(2) is actively depleted by S. flexneri aerobic respiration-and not host neutrophils
57 efficient T3SS translocation of effectors by S. flexneri and other pathogens that use T3SS, Salmonell
58 tes was Shigella sonnei (54.4%), followed by S. flexneri (39.2%), S. boydii (4.1%), and S. dysenteria
59 or IcsA localization and plaque formation by S. flexneri.
60 transepithelial signaling to PMNL induced by S. flexneri.
61                           Apical invasion by S. flexneri is very limited but increases ~10-fold when
62 ependent enhancement of cellular invasion by S. flexneri.
63 l hemagglutinin-tagged spa15 was secreted by S. flexneri within 2 h in the Congo red secretion assay,
64   OspF and OspC1 are known to be secreted by S. flexneri, but their functions are unknown.
65                            In HeLa229 cells, S. flexneri also formed membrane protrusions that extend
66                        Here we characterized S. flexneri actin-based motility in HT-29 intestinal cel
67                    To ensure that the cloned S. flexneri recA gene was not inactivated, it was rescue
68                                 In contrast, S. flexneri invades the large intestine epithelium at th
69 y to ICE and this enzyme is activated during S. flexneri infection.
70 e dependence on the activation of Dia during S. flexneri infection contrasts with the inhibition of t
71 We demonstrate that activation of PKC during S. flexneri infection is attenuated in the absence of PD
72 pecific CD8(+) T cells are not primed during S. flexneri infection and, as a result, afford little pr
73                         The vaccine elicited S. flexneri 2a LPS-specific immunoglobulin A (IgA), IgG,
74 at disruption of HIE tight junctions enables S. flexneri invasion via the apical surface.
75 ion with three distinct growth environments: S. flexneri growing in broth (in vitro), S. flexneri gro
76 eiving single doses of >/=10(4) CFU excreted S. flexneri 2a, and this colonization induced significan
77 ctious process over time with GFP-expressing S. flexneri.
78      Each transposon insertion with flanking S. flexneri DNA was cloned and sequenced.
79 e Gram-negative bacterium Shigella flexneri (S. flexneri) as a first step of bacteriophage infection.
80 uc2 were observed in the enteroids following S. flexneri infection.
81 We demonstrate that NO is produced following S. flexneri infection both in mice and in activated cell
82            The invasin IpaA is essential for S. flexneri pathogenesis and binds to the cytoskeletal p
83 ression and this regulation is important for S. flexneri virulence.
84 d at the bacterial pole that is required for S. flexneri actin-based motility during intracellular in
85  expression of cytochrome bd is required for S. flexneri intracellular survival and virulence.
86 e iron transport gene, sitA, in a screen for S. flexneri genes that are induced in the eukaryotic int
87 and IgA and also in urinary IgA specific for S. flexneri 2a LPS were demonstrated.
88 d within the N-terminal regions of IpaB from S. flexneri and SipB from Salmonella enterica serovar Ty
89  DNA fragment containing the imp operon from S. flexneri SA100 pVP was 96% identical to the imp opero
90 nce in stability and is present in pINV from S. flexneri but absent in S. sonnei pINV.
91                       Signals resulting from S. flexneri interactions with subcapsular sinus macropha
92 from avian pathogenic E. coli, and SepA from S. flexneri.
93 The activation of apoptosis by BLP shed from S. flexneri is discussed as a novel aspect of the intera
94 ar octamers, whereas the wild-type WzzB from S. flexneri was found to be an open trimer.
95 nto culture supernatants of actively growing S. flexneri.
96              In order to thrive in the host, S. flexneri must adapt to environmental conditions in th
97                      To test our hypothesis, S. flexneri strain 2457T was subcultured in media contai
98 icroarray analysis was performed to identify S. flexneri genes differentially regulated by the NtrBC
99 hysiological effects of iron availability in S. flexneri.
100 of both of these systems were constructed in S. flexneri.
101      A sitA::cam mutation was constructed in S. flexneri.
102 ction/repression ratios of up to 240-fold in S. flexneri and up to 50-fold in K. pneumoniae.
103     Characterization of the sitABCD genes in S. flexneri indicates that they encode a ferrous iron tr
104 tant in defining the precise role of IpaC in S. flexneri pathogenesis and in exploring the potential
105 and Salmonella, on a pathogenicity island in S. flexneri and S. sonnei and in a different chromosomal
106 may constitute an island within an island in S. flexneri.
107 butes to survival and induced mutagenesis in S. flexneri following exposure to UV radiation.
108 of deletion mutations in the guaBA operon in S. flexneri 2a vaccine strains in clinical studies, we d
109  two genes are part of a virulence operon in S. flexneri.
110 atidylinositol 3-phosphate kinase PIK3C2A in S. flexneri dissemination.
111 nalyses identified genes that are present in S. flexneri isolates but not in the three other Shigella
112    PIK3C2A-mediated PtdIns(3)P production in S. flexneri protrusions was regulated by host cell tyros
113 portant bile salt transcriptional profile in S. flexneri 2457T, including induced drug resistance and
114  of adhesin-like autotransporter proteins in S. flexneri biofilm formation.
115 ously uncharacterized for potential roles in S. flexneri growth within the eukaryotic intracellular e
116  small plasmid pHS-2 play important roles in S. flexneri invasion and virulence.
117 nd gluconeogenic pathways influence steps in S. flexneri invasion and plaque formation.
118 on of the Vps/VacJ ABC transporter system in S. flexneri in both the maintenance of lipid asymmetry i
119 es comprised 89.4% of S. flexneri, including S. flexneri 2a, S. flexneri 6, S. flexneri 3a, S. flexne
120 ng protocol was devised to follow individual S. flexneri in a large tissue volume.
121                               Interestingly, S. flexneri pINV also harbours two putative partitioning
122               Following electroporation into S. flexneri 2a vaccine strain CVD 1204, coexpression of
123 h of these pathways is used by intracellular S. flexneri, mutants were constructed and tested in a pl
124 ng that it is not critical for intracellular S. flexneri.
125  infection of human colonic tissue, invasive S. flexneri interacts with and occasionally invades B ly
126 espectively, of 1130 Shigella case isolates; S. flexneri comprised 65.9% and S. sonnei 23.7%.
127                                  The 120-kDa S. flexneri outer membrane protein IcsA is essential for
128 s in vitro and that while it is able to kill S. flexneri in a cell-free system, it is not required fo
129                  The efficacy of heat-killed S. flexneri 2a was enhanced only by mutant LT molecules.
130 onfirmed the bias of experimentally measured S. flexneri for early crypt targeting.
131    After S. flexneri invades HIE monolayers, S. flexneri replicates within HIE cells and forms actin
132 ession profiles of wild type and dksA mutant S. flexneri determined that hfq expression was reduced i
133               They characterized tgt- mutant S. flexneri strains in which the translation of VirF is
134 igella flexneri 2a vaccine comprising native S. flexneri 2a lipopolysaccharide (LPS) complexed to men
135 ed by TB&S as S. boydii due to nonfunctional S. flexneri O antigen biosynthesis genes.
136  We conclude that neither D. radiodurans nor S. flexneri RecA is functional in the other species, nor
137 ve serotypes/subserotypes comprised 89.4% of S. flexneri, including S. flexneri 2a, S. flexneri 6, S.
138 n of NOD2 or EGFR compromises the ability of S. flexneri to induce IDO1 expression.
139 EF-P or PoxA leads to an impaired ability of S. flexneri to invade epithelial cells and form plaques
140 DegP is a protease, the protease activity of S. flexneri DegP was not required for IcsA localization
141                                  Analysis of S. flexneri mutants showed that invasion and a functiona
142 Specific parameters included the analysis of S. flexneri positions relative to the epithelial surface
143  submucosa, which are fundamental aspects of S. flexneri pathogenesis.
144 ime points, there was a clear association of S. flexneri with crypts, key morphological features of t
145 ies prevalence was not static, with cases of S. flexneri infection in men decreasing between 2015 and
146 f the Enterobacteriaceae Characterization of S. flexneri 2457T biofilms determined that both bile sal
147              Biochemical characterization of S. flexneri EP and culture supernatants, including enzym
148  system, it is not required for clearance of S. flexneri in either infected mice or in activated cell
149             The active needle tip complex of S. flexneri is composed of a tip protein, IpaD, and two
150 l dissemination as a critical determinant of S. flexneri pathogenesis and provides a unique small-ani
151 und in human colostrum blocks development of S. flexneri-induced inflammatory enteritis.
152    Throughout the study period, diagnoses of S. flexneri and S. sonnei infections were most common in
153 tion, but are required for stable docking of S. flexneri to cells; moreover, stable docking triggers
154                             The effectors of S. flexneri invasion are the Ipa proteins, particularly
155 tivities and may be responsible for entry of S. flexneri into target cells.
156  the S. flexneri serotypes tested (except of S. flexneri serotype 6) as assessed by enzyme-linked imm
157      These results indicate that exposure of S. flexneri to conditions favoring induction of the viru
158 tive immunity, we investigated the impact of S. flexneri on T-cell dynamics in vivo.
159 ue samples further confirmed the location of S. flexneri within colonocytes at the mouth of crypts.
160                        We suggest a model of S. flexneri dissemination in which the formation of VLPs
161 tors CsrA and Cra in a cell culture model of S. flexneri virulence.
162 , severely inhibited actin-based motility of S. flexneri (no motility observed in the majority of exp
163 completely inhibited actin-based motility of S. flexneri while only moderately inhibiting motility of
164 rain pWR700, an ipaH(7.8) deletion mutant of S. flexneri 2a strain 2457T, behaved like the wild-type
165 helial cells with an ospZ deletion mutant of S. flexneri resulted in reduced PMN transepithelial migr
166               Furthermore, an IcsA mutant of S. flexneri that cannot interact with the cytoskeleton a
167                   An rpoS deletion mutant of S. flexneri was also constructed to confirm the importan
168  invasion plasmid antigen B (ipaB) mutant of S. flexneri, hemolysin (hly) and positive-regulatory fac
169 store invasiveness to an ipaC null mutant of S. flexneri, the N-terminus is essential, because IpaC m
170 pH and to promote entry by an ipaC mutant of S. flexneri.
171 at rough lipopolysaccharide (LPS) mutants of S. flexneri 2a are avirulent and cannot form plaques in
172 d thus compromises the invasive phenotype of S. flexneri.
173 ted through genes on the invasion plasmid of S. flexneri M90T, since BS176, cured of plasmid, behaves
174 ive information regarding the progression of S. flexneri infection in an unbiased and exhaustive mann
175 ms by which each of the two MsbB proteins of S. flexneri likely contributes to pathogenesis.
176        Pyruvate increased the growth rate of S. flexneri in vitro, suggesting that it may be a prefer
177 ability to form fireworks, the rfb region of S. flexneri 2a was replaced with the rfb region from Esc
178                   The amino acid sequence of S. flexneri type 1 FimA contained 18 substitutions compa
179 3766-3770, 2011) for molecular serotyping of S. flexneri This study was performed by seven internatio
180 more, MD) for confirmation and serotyping of S. flexneri; one-third of isolates were sent to the Cent
181  report that OspB can be added to the set of S. flexneri T3SS effectors required to modulate the inna
182 ce and contributes to cell-to-cell spread of S. flexneri in cell culture.
183  for efficient entry and cell-cell spread of S. flexneri, whereas the lower affinity VBS appears to c
184 ons, in turn allowing cell-to-cell spread of S. flexneri.
185 wild-type intracellular growth and spread of S. flexneri.
186 eworks formation, we constructed a strain of S. flexneri (BS497) that contains a mutation in rfc, enc
187 ized genes, such as an ipaB mutant strain of S. flexneri and an hly mutant strain of L. monocytogenes
188                                   Strains of S. flexneri and Escherichia coli that carry derivatives
189 hylogenetic relationships between strains of S. flexneri WGS data provided both genome-derived seroty
190 . sonnei plasmid is less stable than that of S. flexneri, especially at environmental temperatures.
191 een when vciB was expressed in an E. coli or S. flexneri strain defective for the ferrous iron transp
192        Lipid A from V. fischeri, E. coli, or S. flexneri induced apoptosis.
193 for infection by the T3SS-dependent pathogen S. flexneri.
194 nsistent with a reduced endotoxic potential, S. flexneri 2a msbB mutants were attenuated in an acute
195 etent for tyrosine kinase signaling promotes S. flexneri dissemination in epithelial cells.
196 nses to intranasally administered proteosome-S. flexneri 2a LPS vaccine is similar to those reported
197 dentical activity was identified in purified S. flexneri endotoxin, defined here as a mixture of lipo
198 o compared with that of a recently sequenced S. flexneri 2a strain, 301.
199 the use of this molecular method to serotype S. flexneri and showed several advantages over the tradi
200 s to evaluate a real-time PCR for serotyping S. flexneri and to use whole-genome sequencing (WGS) to
201  (rare) remaining subserotype through shared S. flexneri group antigens.
202 lent vaccine with O antigens from S. sonnei, S. flexneri 2a, S. flexneri 3a, and S. flexneri 6 can pr
203 embers of each of the four Shigella species: S. flexneri, S. sonnei, S. boydii, and S. dysenteriae.
204   During growth at 37 degrees C, spontaneous S. flexneri mutants arise which have undergone virulence
205   A novel bioluminescent S. flexneri strain (S. flexneri lux1) was generated, which can be used in a
206 ositions relative to the epithelial surface, S. flexneri density within the tissue, and volume of tis
207                              We believe that S. flexneri, like other pathogens, inhibits apoptosis in
208                    Our data demonstrate that S. flexneri 2457T employs multiple mechanisms to survive
209               These results demonstrate that S. flexneri 2a OmpA may play a critical role in the deve
210              We previously demonstrated that S. flexneri inhibits staurosporine-induced apoptosis in
211                 This study demonstrates that S. flexneri cytochrome bd expression is necessary for no
212 unity is initiated, we provide evidence that S. flexneri, via its type III secretion system, impairs
213                           We also found that S. flexneri contained a chromosomally encoded umuDC oper
214 in vivo models of shigellosis, we found that S. flexneri induces the expression of indoleamine 2,3-di
215                 These findings indicate that S. flexneri targets T lymphocytes in vivo and highlight
216                 A previous study showed that S. flexneri forms biofilms in the presence of bile salts
217 ducted in various cell lines, we showed that S. flexneri relies on neural Wiskott-Aldrich Syndrome pr
218 icited and is short-lasting, suggesting that S. flexneri interferes with the priming of specific immu
219 n response to infection, which suggests that S. flexneri infection not only triggers the production o
220                                          The S. flexneri dksA mutant exhibited sensitivity to acid an
221                                          The S. flexneri gene putatively encodes a approximately 90-k
222                                          The S. flexneri sit promoter was repressed by either iron or
223                                          The S. flexneri-specific regions contain many genes that cou
224                             In addition, the S. flexneri lux1 strain was used with an intraperitoneal
225 l antibodies that cross-reacted with all the S. flexneri serotypes tested (except of S. flexneri sero
226 e discovered that Orf212 was secreted by the S. flexneri T3SS and renamed this protein OspZ.
227            Recombinant plasmids carrying the S. flexneri vpsA, -B, and -C genes complemented all of t
228                          Expression from the S. flexneri suf and isc promoters increased when Shigell
229                          In contrast, in the S. flexneri DeltahtrB mutant, a compensatory lipid A pal
230    A mutation in phoB was constructed in the S. flexneri pst mutant, and the phoB mutation suppressed
231  carbon metabolism may be key factors in the S. flexneri transition from the extra- to the intracellu
232 environment, we constructed mutations in the S. flexneri uhpT and pstS genes by allelic exchange.
233  that mxiM, part of the mxi-spa locus in the S. flexneri virulence plasmid, encodes an indispensable
234  radioactive iron by the Feo system into the S. flexneri iron transport mutant was stimulated by the
235                            Comparison of the S. flexneri 2a and laboratory E. coli K-12 genomes in th
236 reened a library containing fragments of the S. flexneri chromosome fused to a promoterless green flu
237                                  Some of the S. flexneri dksA mutant cells showed aberrant localizati
238 rate that the acid sensitivity defect of the S. flexneri fur mutant is due to repression of ydeP by R
239 ed normal production and localization of the S. flexneri IcsA protein.
240     This suggested that the inability of the S. flexneri pst mutant to form wild-type plaques in Henl
241                            Expression of the S. flexneri sit and mntH promoters was higher when Shige
242       The deduced amino acid sequence of the S. flexneri sit locus was homologous to the Salmonella e
243 signaling and relied on the integrity of the S. flexneri type 3 secretion system (T3SS).
244 tants was due to decreased expression of the S. flexneri virulence factor regulators virF and virB, r
245 ng either E. coli or V. cholerae Feo, or the S. flexneri ferrous iron transport system Sit, restored
246 tibiotic treatment significantly reduced the S. flexneri infection.
247      BLAST search analysis revealed that the S. flexneri 2457T genome harbors 4 genes, S1242, S1289,
248                                    Thus, the S. flexneri type III secretion system can be induced in
249               Serum antibody response to the S. flexneri 2a O antigen, the primary antigen for protec
250 aC that restores partial invasiveness to the S. flexneri ipaC null mutant also restores full contact-
251              IpaC is then transported to the S. flexneri surface when target cell lipids are added, a
252 cretion induction or IpaC recruitment to the S. flexneri surface.
253 he Escherichia coli TGT (99% identity to the S. flexneri TGT) in vitro.
254                                   Therefore, S. flexneri infection induces a global blockage of host
255 sit genes provide a competitive advantage to S. flexneri growing within epithelial cells, and a sitA
256 bronchopulmonary model, adaptive immunity to S. flexneri 2a is an antibody-mediated, B-lymphocyte-dep
257  fail to play a role in adaptive immunity to S. flexneri, we investigated whether antigen-specific CD
258 ponses are important to adaptive immunity to S. flexneri.
259  an important function of GBP recruitment to S. flexneri is to prevent the spread of infection to nei
260  A antibody-secreting cell (ASC) response to S. flexneri 2a O-specific lipopolysaccharide was seen, w
261 ivity was significantly lower in response to S. flexneri 2a than E. coli LPS and further decreased in
262 ive serum immunoglobulin A (IgA) response to S. flexneri lipopolysaccharide.
263  lower (approximately 20-90%) in response to S. flexneri than to E. coli LPS/lipid A and PBMC from po
264 sed during invasion and that are specific to S. flexneri.
265                               We transformed S. flexneri with a plasmid that expresses a two-hemagglu
266                                          Two S. flexneri chromosomal loci that are required for these
267  work, we report the multiple effects of two S. flexneri effectors, IpaJ and VirA, which target small
268        This strategy involves the use of two S. flexneri serotypes (2a and 3a), which together bear t
269  oral vaccine strain prepared from wild-type S. flexneri 2a by rational use of recombinant DNA techno
270 protected against a challenge with wild-type S. flexneri 2a in a keratoconjunctivitis Sereny test.
271 ce plasmid-cured derivative of the wild-type S. flexneri 2a isolate 2457T.
272 were protected from challenge with wild-type S. flexneri 2a.
273                 Interestingly, the wild-type S. flexneri also formed larger plaques in the presence o
274 found to: (i) enhance the entry of wild-type S. flexneri and S. typhimurium into cultured cells; (ii)
275 aller plaques than those formed by wild-type S. flexneri in confluent monolayers of Henle and Caco-2
276 er challenged (Sereny test) with a wild-type S. flexneri serotype 1a, 1b, 2b, 4b, 5b, Y, or 6 strain
277 to that of T84 cells infected with wild-type S. flexneri.
278 in confluent monolayers similar to wild-type S. flexneri.
279  protection against challenge with wild-type S. flexneri.
280 e, interacts with downstream effectors under S. flexneri infection.
281                                        Using S. flexneri as an infection model in human epithelial ce
282 omplementation analyses were conducted using S. flexneri SF621 and S. typhimurium SB220, neither of w
283                            Of note, virulent S. flexneri 2a could invade and colonize not only system
284 re challenged with 2 x 10(3) CFU of virulent S. flexneri 2a organisms.
285 paD failed to enhance the uptake of virulent S. flexneri and did not facilitate uptake of BS103.
286 udy, intraperitoneal challenge with virulent S. flexneri 2a (YSH6000) resulted in diarrhea and severe
287 that intraperitoneal challenge with virulent S. flexneri 2a can provoke bacillary dysentery and sever
288 llowing conjunctival challenge with virulent S. flexneri 2a strain 2457T.
289 ts: S. flexneri growing in broth (in vitro), S. flexneri growing within epithelial cell cytoplasm (in
290 neri or S. boydii by the kmer ID, and 8 were S. flexneri isolates misidentified by TB&S as S. boydii
291 ttenuated strains used in these studies were S. flexneri 2a strain CVD 1207 (DeltaguaB-A DeltavirG De
292 at had a higher level of gfp expression when S. flexneri was intracellular (in Henle cells) than when
293 was intracellular (in Henle cells) than when S. flexneri was extracellular (in Luria-Bertani broth) w
294 ch IpaA subverts vinculin's functions, where S. flexneri utilizes a remarkable level of molecular mim
295 ignificant protection against challenge with S. flexneri serotypes 1b, 2b, 5b, and Y but not with ser
296 d to investigate if HeLa cells infected with S. flexneri are able to resist the induction of apoptosi
297 ilar to humans, infant rabbits infected with S. flexneri experience severe inflammation, massive ulce
298 munofluorescence of HeLa cells infected with S. flexneri expressing OspF-2HA or OspC1-2HA revealed th
299 lial migration in response to infection with S. flexneri was dependent on 12/15-LOX activity, the enz
300                We show that vaccination with S. flexneri serotype 2a confers protection to mice that

 
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