ライフサイエンスコーパス: S. flexneri

1 S. flexneri actin-based motility has been characterized

2 S. flexneri dissemination in HT-29 cells led to the loca

3 S. flexneri mutants that contain a disruption in the cyd

4 S. flexneri secretes effector proteins into the eukaryot

5 S. flexneri skp and surA mutants failed to form plaques

6 S. flexneri strains containing deletion mutations in the

7 S. flexneri uses a type III secretion system to inject e

8 S. flexneri-infected cells were used as a control.

9 accine must protect against S. sonnei and 15 S. flexneri serotypes/subserotypes.

10 cryptic prophages, 372 pseudogenes, and 195 S. flexneri-specific genes.

11 Disruption of icsP in serotype 2a S. flexneri leads to a marked reduction in IcsA cleavage

12 ctin-based motility of wild-type serotype 2a S. flexneri.

13 h O antigens from S. sonnei, S. flexneri 2a, S. flexneri 3a, and S. flexneri 6 can provide broad dire

14 4% of S. flexneri, including S. flexneri 2a, S. flexneri 6, S. flexneri 3a, S. flexneri 2b, and S. fl

15 flexneri 2a, S. flexneri 6, S. flexneri 3a, S. flexneri 2b, and S. flexneri 1b.

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

17 report represents the first description of a S. flexneri gene identified based on enhanced expression

18 Addition of this pstA(R220Q) mutation to a S. flexneri pst mutant, as part of the pst operon, resto

19 important physiological signals to activate S. flexneri 2457T virulence.

20 We identified an additional S. flexneri putative iron transport gene, sitA, in a scr

21 linked immunosorbent assay responses against S. flexneri 2a lipopolysaccharide in two-thirds of the v

22 2-hybridizing sequences were detected in all S. flexneri strains tested and parts of the island were

23 Although S. flexneri causes most disease in low-income countries

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

25 f O-glucosylation patterns encountered among S. flexneri type-specific polysaccharides.

26 An S. flexneri pst mutant forms smaller plaques in Henle ce

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

28 Furthermore, an S. flexneri ydeP mutant was defective for both glutamate

29 However, an S. flexneri rpoS mutant formed plaques on tissue culture

30 xneri 6, S. flexneri 3a, S. flexneri 2b, and S. flexneri 1b.

31 sonnei, S. flexneri 2a, S. flexneri 3a, and S. flexneri 6 can provide broad direct coverage against

32 th shared and unique epitopes on E. coli and S. flexneri type 1 fimbriae.

33 contribute to immune evasion of E. coli and S. flexneri, favoring invasiveness and increasing the se

34 eltaguaB-A DeltavirG Deltaset1 Deltasen) and S. flexneri 3a strain CVD 1211 (DeltaguaB-A DeltavirG De

35 situ structures of the Y. enterocolitica and S. flexneri injectisomes had similar dimensions and were

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

37 ithelial cell cytoplasm (intracellular), and S. flexneri that were cultured with, but did not invade,

38 roys these cells, while L. monocytogenes and S. flexneri appear to be internalized into M cells in a

39 Since attenuated serovar Typhi and S. flexneri can deliver measles DNA vaccines mucosally i

40 und that S. enterica serovar Typhimurium and S. flexneri activate different subtypes of phospholipase

41 S. enterica serovar Typhimurium and S. flexneri cell entry was dependent on the Salmonella p

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

43 although S. enterica serovar Typhimurium and S. flexneri utilize different mechanisms for triggering

44 hat both S. enterica serovar Typhimurium and S. flexneri were located in intracellular niches in ES c

45 re not interchangeable in S. typhimurium and S. flexneri.

46 ed mucosal IgA (in tears) and serum IgG anti-S. flexneri 2a O antibodies.

47 nterrupted in the same open reading frame as S. flexneri ispA.

48 SC602 is the first example of an attenuated S. flexneri 2a candidate vaccine that provides protectio

49 ortantly, mice prevaccinated with attenuated S. flexneri 2a (SC602) strain were protected against int

50 mmon origin for the aerobactin genes in both S. flexneri and E. coli pColV.

51 is shown here that clinical isolates of both S. flexneri and Shigella sonnei invade epithelial cells

52 ection of epithelial cells from apoptosis by S. flexneri is regulated by one or more of the bacterial

53 efficient T3SS translocation of effectors by S. flexneri and other pathogens that use T3SS, Salmonell

54 or IcsA localization and plaque formation by S. flexneri.

55 transepithelial signaling to PMNL induced by S. flexneri.

56 ependent enhancement of cellular invasion by S. flexneri.

57 l hemagglutinin-tagged spa15 was secreted by S. flexneri within 2 h in the Congo red secretion assay,

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

59 In HeLa229 cells, S. flexneri also formed membrane protrusions that extend

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

61 To ensure that the cloned S. flexneri recA gene was not inactivated, it was rescue

62 In contrast, S. flexneri invades the large intestine epithelium at th

63 y to ICE and this enzyme is activated during S. flexneri infection.

64 e dependence on the activation of Dia during S. flexneri infection contrasts with the inhibition of t

65 We demonstrate that activation of PKC during S. flexneri infection is attenuated in the absence of PD

66 pecific CD8(+) T cells are not primed during S. flexneri infection and, as a result, afford little pr

67 The vaccine elicited S. flexneri 2a LPS-specific immunoglobulin A (IgA), IgG,

68 ion with three distinct growth environments: S. flexneri growing in broth (in vitro), S. flexneri gro

69 eiving single doses of >/=10(4) CFU excreted S. flexneri 2a, and this colonization induced significan

70 ctious process over time with GFP-expressing S. flexneri.

71 Each transposon insertion with flanking S. flexneri DNA was cloned and sequenced.

72 e Gram-negative bacterium Shigella flexneri (S. flexneri) as a first step of bacteriophage infection.

73 We demonstrate that NO is produced following S. flexneri infection both in mice and in activated cell

74 The invasin IpaA is essential for S. flexneri pathogenesis and binds to the cytoskeletal p

75 ression and this regulation is important for S. flexneri virulence.

76 expression of cytochrome bd is required for S. flexneri intracellular survival and virulence.

77 e iron transport gene, sitA, in a screen for S. flexneri genes that are induced in the eukaryotic int

78 and IgA and also in urinary IgA specific for S. flexneri 2a LPS were demonstrated.

79 d within the N-terminal regions of IpaB from S. flexneri and SipB from Salmonella enterica serovar Ty

80 DNA fragment containing the imp operon from S. flexneri SA100 pVP was 96% identical to the imp opero

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

82 Signals resulting from S. flexneri interactions with subcapsular sinus macropha

83 from avian pathogenic E. coli, and SepA from S. flexneri.

84 The activation of apoptosis by BLP shed from S. flexneri is discussed as a novel aspect of the intera

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

86 nto culture supernatants of actively growing S. flexneri.

87 In order to thrive in the host, S. flexneri must adapt to environmental conditions in th

88 To test our hypothesis, S. flexneri strain 2457T was subcultured in media contai

89 icroarray analysis was performed to identify S. flexneri genes differentially regulated by the NtrBC

90 hysiological effects of iron availability in S. flexneri.

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

92 A sitA::cam mutation was constructed in S. flexneri.

93 ction/repression ratios of up to 240-fold in S. flexneri and up to 50-fold in K. pneumoniae.

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

95 tant in defining the precise role of IpaC in S. flexneri pathogenesis and in exploring the potential

96 and Salmonella, on a pathogenicity island in S. flexneri and S. sonnei and in a different chromosomal

97 may constitute an island within an island in S. flexneri.

98 butes to survival and induced mutagenesis in S. flexneri following exposure to UV radiation.

99 of deletion mutations in the guaBA operon in S. flexneri 2a vaccine strains in clinical studies, we d

100 two genes are part of a virulence operon in S. flexneri.

101 atidylinositol 3-phosphate kinase PIK3C2A in S. flexneri dissemination.

102 nalyses identified genes that are present in S. flexneri isolates but not in the three other Shigella

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

104 portant bile salt transcriptional profile in S. flexneri 2457T, including induced drug resistance and

105 te that the expression of acid resistance in S. flexneri may be multifactorial and involve proteins l

106 ously uncharacterized for potential roles in S. flexneri growth within the eukaryotic intracellular e

107 small plasmid pHS-2 play important roles in S. flexneri invasion and virulence.

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

109 on of the Vps/VacJ ABC transporter system in S. flexneri in both the maintenance of lipid asymmetry i

110 es comprised 89.4% of S. flexneri, including S. flexneri 2a, S. flexneri 6, S. flexneri 3a, S. flexne

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

112 Following electroporation into S. flexneri 2a vaccine strain CVD 1204, coexpression of

113 h of these pathways is used by intracellular S. flexneri, mutants were constructed and tested in a pl

114 ng that it is not critical for intracellular S. flexneri.

115 infection of human colonic tissue, invasive S. flexneri interacts with and occasionally invades B ly

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

117 The 120-kDa S. flexneri outer membrane protein IcsA is essential for

118 s in vitro and that while it is able to kill S. flexneri in a cell-free system, it is not required fo

119 The efficacy of heat-killed S. flexneri 2a was enhanced only by mutant LT molecules.

120 onfirmed the bias of experimentally measured S. flexneri for early crypt targeting.

121 ession profiles of wild type and dksA mutant S. flexneri determined that hfq expression was reduced i

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

123 igella flexneri 2a vaccine comprising native S. flexneri 2a lipopolysaccharide (LPS) complexed to men

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

125 appears to promote uptake of the noninvasive S. flexneri 2a strain BS103.

126 We conclude that neither D. radiodurans nor S. flexneri RecA is functional in the other species, nor

127 ve serotypes/subserotypes comprised 89.4% of S. flexneri, including S. flexneri 2a, S. flexneri 6, S.

128 EF-P or PoxA leads to an impaired ability of S. flexneri to invade epithelial cells and form plaques

129 DegP is a protease, the protease activity of S. flexneri DegP was not required for IcsA localization

130 Analysis of S. flexneri mutants showed that invasion and a functiona

131 Specific parameters included the analysis of S. flexneri positions relative to the epithelial surface

132 submucosa, which are fundamental aspects of S. flexneri pathogenesis.

133 ime points, there was a clear association of S. flexneri with crypts, key morphological features of t

134 f the Enterobacteriaceae Characterization of S. flexneri 2457T biofilms determined that both bile sal

135 Biochemical characterization of S. flexneri EP and culture supernatants, including enzym

136 system, it is not required for clearance of S. flexneri in either infected mice or in activated cell

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

138 und in human colostrum blocks development of S. flexneri-induced inflammatory enteritis.

139 tion, but are required for stable docking of S. flexneri to cells; moreover, stable docking triggers

140 The three proposed effectors of S. flexneri internalization are invasion plasmid antigen

141 The effectors of S. flexneri invasion are the Ipa proteins, particularly

142 tivities and may be responsible for entry of S. flexneri into target cells.

143 the S. flexneri serotypes tested (except of S. flexneri serotype 6) as assessed by enzyme-linked imm

144 These results indicate that exposure of S. flexneri to conditions favoring induction of the viru

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

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

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

148 tors CsrA and Cra in a cell culture model of S. flexneri virulence.

149 , severely inhibited actin-based motility of S. flexneri (no motility observed in the majority of exp

150 completely inhibited actin-based motility of S. flexneri while only moderately inhibiting motility of

151 rain pWR700, an ipaH(7.8) deletion mutant of S. flexneri 2a strain 2457T, behaved like the wild-type

152 helial cells with an ospZ deletion mutant of S. flexneri resulted in reduced PMN transepithelial migr

153 Furthermore, an IcsA mutant of S. flexneri that cannot interact with the cytoskeleton a

154 An rpoS deletion mutant of S. flexneri was also constructed to confirm the importan

155 invasion plasmid antigen B (ipaB) mutant of S. flexneri, hemolysin (hly) and positive-regulatory fac

156 store invasiveness to an ipaC null mutant of S. flexneri, the N-terminus is essential, because IpaC m

157 pH and to promote entry by an ipaC mutant of S. flexneri.

158 at rough lipopolysaccharide (LPS) mutants of S. flexneri 2a are avirulent and cannot form plaques in

159 s we isolated five acid-sensitive mutants of S. flexneri, which had lost their ability to survive at

160 d thus compromises the invasive phenotype of S. flexneri.

161 ted through genes on the invasion plasmid of S. flexneri M90T, since BS176, cured of plasmid, behaves

162 ive information regarding the progression of S. flexneri infection in an unbiased and exhaustive mann

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

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

165 ability to form fireworks, the rfb region of S. flexneri 2a was replaced with the rfb region from Esc

166 The amino acid sequence of S. flexneri type 1 FimA contained 18 substitutions compa

167 more, MD) for confirmation and serotyping of S. flexneri; one-third of isolates were sent to the Cent

168 report that OspB can be added to the set of S. flexneri T3SS effectors required to modulate the inna

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

170 for efficient entry and cell-cell spread of S. flexneri, whereas the lower affinity VBS appears to c

171 ons, in turn allowing cell-to-cell spread of S. flexneri.

172 wild-type intracellular growth and spread of S. flexneri.

173 eworks formation, we constructed a strain of S. flexneri (BS497) that contains a mutation in rfc, enc

174 ized genes, such as an ipaB mutant strain of S. flexneri and an hly mutant strain of L. monocytogenes

175 Strains of S. flexneri and Escherichia coli that carry derivatives

176 hylogenetic relationships between strains of S. flexneri WGS data provided both genome-derived seroty

177 . sonnei plasmid is less stable than that of S. flexneri, especially at environmental temperatures.

178 cells with purified IpaC enhances uptake of S. flexneri by host cells.

179 een when vciB was expressed in an E. coli or S. flexneri strain defective for the ferrous iron transp

180 Lipid A from V. fischeri, E. coli, or S. flexneri induced apoptosis.

181 for infection by the T3SS-dependent pathogen S. flexneri.

182 nsistent with a reduced endotoxic potential, S. flexneri 2a msbB mutants were attenuated in an acute

183 etent for tyrosine kinase signaling promotes S. flexneri dissemination in epithelial cells.

184 nses to intranasally administered proteosome-S. flexneri 2a LPS vaccine is similar to those reported

185 dentical activity was identified in purified S. flexneri endotoxin, defined here as a mixture of lipo

186 o compared with that of a recently sequenced S. flexneri 2a strain, 301.

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

188 (rare) remaining subserotype through shared S. flexneri group antigens.

189 lent vaccine with O antigens from S. sonnei, S. flexneri 2a, S. flexneri 3a, and S. flexneri 6 can pr

190 embers of each of the four Shigella species: S. flexneri, S. sonnei, S. boydii, and S. dysenteriae.

191 During growth at 37 degrees C, spontaneous S. flexneri mutants arise which have undergone virulence

192 ositions relative to the epithelial surface, S. flexneri density within the tissue, and volume of tis

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

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

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

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

197 This study demonstrates that S. flexneri cytochrome bd expression is necessary for no

198 unity is initiated, we provide evidence that S. flexneri, via its type III secretion system, impairs

199 We also found that S. flexneri contained a chromosomally encoded umuDC oper

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

201 ducted in various cell lines, we showed that S. flexneri relies on neural Wiskott-Aldrich Syndrome pr

202 icited and is short-lasting, suggesting that S. flexneri interferes with the priming of specific immu

203 n response to infection, which suggests that S. flexneri infection not only triggers the production o

204 The S. flexneri dksA mutant exhibited sensitivity to acid an

205 The S. flexneri gene putatively encodes a approximately 90-k

206 The S. flexneri sit promoter was repressed by either iron or

207 The S. flexneri-specific regions contain many genes that cou

208 l antibodies that cross-reacted with all the S. flexneri serotypes tested (except of S. flexneri sero

209 e discovered that Orf212 was secreted by the S. flexneri T3SS and renamed this protein OspZ.

210 Recombinant plasmids carrying the S. flexneri vpsA, -B, and -C genes complemented all of t

211 Expression from the S. flexneri suf and isc promoters increased when Shigell

212 In contrast, in the S. flexneri DeltahtrB mutant, a compensatory lipid A pal

213 A mutation in phoB was constructed in the S. flexneri pst mutant, and the phoB mutation suppressed

214 carbon metabolism may be key factors in the S. flexneri transition from the extra- to the intracellu

215 environment, we constructed mutations in the S. flexneri uhpT and pstS genes by allelic exchange.

216 that mxiM, part of the mxi-spa locus in the S. flexneri virulence plasmid, encodes an indispensable

217 radioactive iron by the Feo system into the S. flexneri iron transport mutant was stimulated by the

218 Comparison of the S. flexneri 2a and laboratory E. coli K-12 genomes in th

219 reened a library containing fragments of the S. flexneri chromosome fused to a promoterless green flu

220 Some of the S. flexneri dksA mutant cells showed aberrant localizati

221 rate that the acid sensitivity defect of the S. flexneri fur mutant is due to repression of ydeP by R

222 ed normal production and localization of the S. flexneri IcsA protein.

223 This suggested that the inability of the S. flexneri pst mutant to form wild-type plaques in Henl

224 Despite a large accumulation of the S. flexneri RecA in D. radiodurans, there is no compleme

225 Expression of the S. flexneri sit and mntH promoters was higher when Shige

226 The deduced amino acid sequence of the S. flexneri sit locus was homologous to the Salmonella e

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

228 tants was due to decreased expression of the S. flexneri virulence factor regulators virF and virB, r

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

230 Thus, the S. flexneri type III secretion system can be induced in

231 Serum antibody response to the S. flexneri 2a O antigen, the primary antigen for protec

232 aC that restores partial invasiveness to the S. flexneri ipaC null mutant also restores full contact-

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

234 cretion induction or IpaC recruitment to the S. flexneri surface.

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

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

237 bronchopulmonary model, adaptive immunity to S. flexneri 2a is an antibody-mediated, B-lymphocyte-dep

238 fail to play a role in adaptive immunity to S. flexneri, we investigated whether antigen-specific CD

239 ponses are important to adaptive immunity to S. flexneri.

240 an important function of GBP recruitment to S. flexneri is to prevent the spread of infection to nei

241 A antibody-secreting cell (ASC) response to S. flexneri 2a O-specific lipopolysaccharide was seen, w

242 ivity was significantly lower in response to S. flexneri 2a than E. coli LPS and further decreased in

243 ive serum immunoglobulin A (IgA) response to S. flexneri lipopolysaccharide.

244 lower (approximately 20-90%) in response to S. flexneri than to E. coli LPS/lipid A and PBMC from po

245 3 induced immunoglobulin G seroconversion to S. flexneri 2a lipopolysaccharide (LPS) in 30, 45, and 3

246 sed during invasion and that are specific to S. flexneri.

247 We transformed S. flexneri with a plasmid that expresses a two-hemagglu

248 Two S. flexneri chromosomal loci that are required for these

249 This strategy involves the use of two S. flexneri serotypes (2a and 3a), which together bear t

250 oral vaccine strain prepared from wild-type S. flexneri 2a by rational use of recombinant DNA techno

251 protected against a challenge with wild-type S. flexneri 2a in a keratoconjunctivitis Sereny test.

252 ce plasmid-cured derivative of the wild-type S. flexneri 2a isolate 2457T.

253 Upon Sereny test challenge with wild-type S. flexneri 2a, CVD 1205-vaccinated animals were signifi

254 were protected from challenge with wild-type S. flexneri 2a.

255 Interestingly, the wild-type S. flexneri also formed larger plaques in the presence o

256 found to: (i) enhance the entry of wild-type S. flexneri and S. typhimurium into cultured cells; (ii)

257 n virG and aroA markedly attenuate wild-type S. flexneri but preserve immunogenicity; however, less r

258 aller plaques than those formed by wild-type S. flexneri in confluent monolayers of Henle and Caco-2

259 er challenged (Sereny test) with a wild-type S. flexneri serotype 1a, 1b, 2b, 4b, 5b, Y, or 6 strain

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

261 in confluent monolayers similar to wild-type S. flexneri.

262 protection against challenge with wild-type S. flexneri.

263 omplementation analyses were conducted using S. flexneri SF621 and S. typhimurium SB220, neither of w

264 Of note, virulent S. flexneri 2a could invade and colonize not only system

265 ighly concentrated water extract of virulent S. flexneri 2a (strain 2457T).

266 re challenged with 2 x 10(3) CFU of virulent S. flexneri 2a organisms.

267 paD failed to enhance the uptake of virulent S. flexneri and did not facilitate uptake of BS103.

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

269 that intraperitoneal challenge with virulent S. flexneri 2a can provoke bacillary dysentery and sever

270 llowing conjunctival challenge with virulent S. flexneri 2a strain 2457T.

271 Infection with virulent S. flexneri results in massive numbers of apoptotic cell

272 ts: S. flexneri growing in broth (in vitro), S. flexneri growing within epithelial cell cytoplasm (in

273 neri or S. boydii by the kmer ID, and 8 were S. flexneri isolates misidentified by TB&S as S. boydii

274 ttenuated strains used in these studies were S. flexneri 2a strain CVD 1207 (DeltaguaB-A DeltavirG De

275 at had a higher level of gfp expression when S. flexneri was intracellular (in Henle cells) than when

276 was intracellular (in Henle cells) than when S. flexneri was extracellular (in Luria-Bertani broth) w

277 ch IpaA subverts vinculin's functions, where S. flexneri utilizes a remarkable level of molecular mim

278 ignificant protection against challenge with S. flexneri serotypes 1b, 2b, 5b, and Y but not with ser

279 d to investigate if HeLa cells infected with S. flexneri are able to resist the induction of apoptosi

280 ells in rabbit Peyer's patches infected with S. flexneri by detecting cells with fragmented DNA.

281 munofluorescence of HeLa cells infected with S. flexneri expressing OspF-2HA or OspC1-2HA revealed th

282 o the cytoplasm of macrophages infected with S. flexneri.

283 lial migration in response to infection with S. flexneri was dependent on 12/15-LOX activity, the enz

284 We show that vaccination with S. flexneri serotype 2a confers protection to mice that