ライフサイエンスコーパス: V. cholerae

1 V. cholerae employs the second messenger molecule 3',5'-

2 V. cholerae forms matrix-encased aggregates, known as bi

3 V. cholerae has a characteristic curved rod morphology,

4 V. cholerae is capable of forming biofilms on solid surf

5 V. cholerae lacking PBP1b or LpoB exhibited wild-type gr

6 V. cholerae mutant strains carrying inactivated AI synth

7 V. cholerae mutants containing the U5C, U7C UTR variant

8 V. cholerae type VI secretion system genes are encoded i

9 V. cholerae's CAI-1 quorum sensing (QS) system is also r

10 V. cholerae, a bacterium that utilizes linearized Ent, c

11 V. cholerae, the causative agent of cholera, is able to

12 We probed microarrays containing 3652 V. cholerae antigens with plasma and antibody-in-lymphoc

13 omonas hydrophila VolA homolog complements a V. cholerae VolA mutant in growth on lysophosphatidylcho

14 lc is able to rescue the biofilm defect of a V. cholerae Deltamlc mutant.

15 Subsequent screening of a V. cholerae genomic library suggested that sigma(E) stre

16 rs associated with the clinical outcome of a V. cholerae infection but did contain putative genomic i

17 an Hfq-dependent sRNA, and (2) control of a V. cholerae QS phenotype, independent of HapR.

18 efers V. cholerae that produces CAI-1 over a V. cholerae mutant defective for CAI-1 production.

19 upon infection with ΔcrbS or Δacs1 V. cholerae mutants.

20 rocholate, serve as host signals to activate V. cholerae virulence through inducing the activity of t

21 ed the mechanism of how taurocholate affects V. cholerae virulence determinants.

22 to investigate innate immune responses after V. cholerae infection for pups suckled by an immune dam.

23 opment of long-term mucosal immunity against V. cholerae O1.

24 the development of a subunit vaccine against V. cholerae.

25 sively assess the contribution of nearly all V. cholerae genes toward growth in the infant rabbit int

26 Strains harbouring in frame deletions of all V. cholerae genes that are predicted to encode diguanyla

27 Regardless, all V. cholerae strains sequenced to date harbour genes for

28 ends upon the expression of genes that allow V. cholerae to overcome host barriers, including low pH,

29 DacA-1 alone among V. cholerae's LMW PBPs is critical for bacterial growth;

30 conserved gene clusters differ widely among V. cholerae strains, and that immunity proteins encoded

31 ctly discriminated between all Aeromonas and V. cholerae isolates.

32 o be generally conserved between E. coli and V. cholerae, they can be combined into diverse functiona

33 th 25 degrees C in both Escherichia coli and V. cholerae.

34 rr are large, we predict that V. harveyi and V. cholerae Qrr are redundant when the perturbations in

35 led mathematical model of the V. harveyi and V. cholerae sRNA circuits.

36 e concentration of Hfq-Qrr in V. harveyi and V. cholerae.

37 l Vibrio parahaemolyticus, V. vulnificus and V. cholerae and select genes associated with clinical st

38 kes the region an attractive target for anti-V. cholerae drugs.

39 e bacteria experience a temperature shift as V. cholerae transition from contaminated water at lower

40 Subsequently, as V. cholerae alkalinizes its environment in late stationa

41 Screening of all publically available V. cholerae genomes showed that numerous strains possess

42 ministration of the phages up to 24 h before V. cholerae challenge reduces colonization of the intest

43 omotes a more favourable interaction between V. cholerae and an arthropod host by reducing the nutrit

44 storing HapR expression in classical biotype V. cholerae repressed vieSAB transcription by binding to

45 We show that in classical biotype V. cholerae, LeuO cooperates with the nucleoid-associate

46 oB, are all required for iron acquisition by V. cholerae Feo.

47 from patients with severe cholera caused by V. cholerae O1 in Bangladesh and age-, sex-, and ABO-mat

48 Thus, acetate consumption by V. cholerae alters host metabolism, and dietary acetate

49 is pathway are unlikely to be encountered by V. cholerae in aquatic reservoirs or within the human ho

50 own to be important for biofilm formation by V. cholerae.

51 es c-di-GMP binding and biofilm formation by V. cholerae.

52 ome in human THP-1 monocytes and in PBMCs by V. cholerae varies with the biotype and is mediated by b

53 domain AlmG substrate to that synthesized by V. cholerae.

54 ne, freeing the fatty acid moiety for use by V. cholerae.

55 we used classical (O395) and El Tor (C6706) V. cholerae biotypes in growth and biochemical assays.

56 surface adhesion-mediated compression causes V. cholerae biofilms to transition from a 2D branched mo

57 developed for detection of Vibrio cholerae ( V. cholerae ).

58 opose that DNA uptake in naturally competent V. cholerae cells occurs in at least two steps: a pilus-

59 ic antibody responses to the nearly complete V. cholerae O1 protein immunome; it has identified antig

60 In samples containing V. cholerae O139, the antigen was bound to the colloidal

61 In contrast, V. cholerae lacking PBP1a or LpoA exhibited growth defic

62 es in the gastrointestinal tract may control V. cholerae biofilm formation at physiological levels.

63 Conversely, V. cholerae Qrr are redundant because any of its Qrr is

64 During its infectious cycle, V. cholerae experiences fluctuations in temperature with

65 neutrophil recruitment, but DNase-deficient V. cholerae caused more clouds of DNA in the intestinal

66 ssessed for their ability to directly detect V. cholerae O139 using samples dispersed in application

67 roles in maintaining zinc homeostasis during V. cholerae growth and pathogenesis.

68 onged to a phyletic lineage of environmental V. cholerae isolates associated with sporadic cases of g

69 In these environments, V. cholerae copes with fluctuations in salinity and osmo

70 e, using electron cryotomography, we explore V. cholerae's cytoplasmic chemoreceptor array and establ

71 dosomal trafficking induced by extracellular V. cholerae.

72 Two extracellular V. cholerae DNases were not required for neutrophil recr

73 -dependent translation of toxT, facilitating V. cholerae virulence at a relevant environmental condit

74 Finally, V. cholerae strains modified to carry a catalytically in

75 bile salt-dependent virulence activation for V. cholerae The induction of TCP by murine intestinal co

76 in the infant mouse model of cholera and for V. cholerae resistance against bile salts, perhaps due t

77 OhrA is critical for V. cholerae adult mouse colonization but is dispensable

78 ween open and closed states is important for V. cholerae biofilm formation, as RbmA variants with swi

79 l that ZnuABC and ZrgABCDE are important for V. cholerae colonization in both infant and adult mouse

80 Thus, at least for V. cholerae PBP1a pathway mutants, the growth phase of t

81 effector-immunity gene profiles observed for V. cholerae and closely related species.

82 ed pilus (TCP), a type IV pilus required for V. cholerae pathogenesis, is necessary for the secretion

83 w metabolic and physiologic requirements for V. cholerae survival, and by combining transposon-insert

84 uture peacekeeping operations: screening for V. cholerae carriage, administering prophylactic antimic

85 present in the gut is a relevant signal for V. cholerae virulence induction in vivo We further show

86 body protects the intestinal epithelium from V. cholerae infection.

87 esent the dodecameric structure of SpeG from V. cholerae in a ligand-free form in three different con

88 Kinetic characterization of SpeG from V. cholerae showed that it acetylates spermidine and spe

89 study provides mechanistic insight into how V. cholerae can acquire phosphate from extracellular DNA

90 Currently, it is unclear how V. cholerae regulates the expression of genes important

91 Identification of immunogenic V. cholerae antigens could lead to a better understandin

92 Overall, we identified 608 immunoreactive V. cholerae antigens in our screening, 59 of which had h

93 In V. cholerae, type VI secretion is controlled by quorum s

94 tory pathways that control its activation in V. cholerae.

95 he primary direct transcription activator in V. cholerae pathogenicity, its regulation by membrane-lo

96 eported that the virulence activator AphB in V. cholerae is involved in ROS resistance.

97 role in shaping the biofilm architecture in V. cholerae biofilms, and this growth pattern is control

98 decuple mutant of 12 diguanylate cyclases in V. cholerae.

99 ize CrvA, the first curvature determinant in V. cholerae.

100 -GMP accumulation and biofilm development in V. cholerae.

101 sT significantly enhanced rpoS expression in V. cholerae biofilms that do not make HapR.

102 esses the expression of virulence factors in V. cholerae, and it is predicted that the intracellular

103 e, bile resistance, and biofilm formation in V. cholerae Here, we investigated the function of ToxR a

104 a previously undercharacterized function in V. cholerae membrane remodeling.

105 ntestine, increase intracellular c-di-GMP in V. cholerae.

106 study, we identified another OxyR homolog in V. cholerae, which we named OxyR2, and we renamed the pr

107 porter of nucleotides has been identified in V. cholerae, suggesting that in order for the organism t

108 y by wHTH TFs: for example, ToxR and LeuO in V. cholerae; HilA, LeuO, SlyA and OmpR in S.

109 to cleave most peptide chain cross-links in V. cholerae's PG.

110 ge compensation, abolishes Qrr redundancy in V. cholerae.

111 haracterize a compatible solute regulator in V. cholerae and couples the regulation of osmotic tolera

112 tion and antimicrobial peptide resistance in V. cholerae.

113 his LPS modification plays a pivotal role in V. cholerae resistance to antimicrobial peptides, weapon

114 e new insights into the role of RS1varphi in V. cholerae evolution and the emergence of highly pathog

115 terminants, we performed a genetic screen in V. cholerae-infected Drosophila and identified the two-c

116 ransduction pathway that is nearly silent in V. cholerae of the El Tor biotype.

117 tation of the transcriptional start sites in V. cholerae and highlight the importance of posttranscri

118 imited the role of natural transformation in V. cholerae.

119 , we systematically dissect PTS transport in V. cholerae.

120 additional, unidentified iron transporter in V. cholerae.

121 f the outer membrane protein, OmpU, which in V. cholerae is proposed to be the sole activator of RpoE

122 nto the mechanism by which bile salts induce V. cholerae virulence but also suggest a means by which

123 monovalent 2D6 Fab fragments also inhibited V. cholerae motility, demonstrating that antibody-mediat

124 rmine acts as an exogenous cue that inhibits V. cholerae biofilm formation through the NspS-MbaA sign

125 Within the intestine, V. cholerae express cholera toxin (CT) and toxin-coregul

126 To avoid self-intoxication, V. cholerae expresses an anti-toxin encoded immediately

127 comparative analyses suggest that DacA-1 is V. cholerae's principal DD-carboxypeptidase.

128 s, and 7436 deaths from cholera and isolated V. cholerae O1 from 1675 of 2703 stool specimens tested

129 regimens can provide protection against live V. cholerae challenge in the suckling mouse model of cho

130 dynamics of individual TcpP proteins in live V. cholerae cells with < 40 nm spatial resolution on a 5

131 Here we have shown that, like E. coli Mlc, V. cholerae Mlc represses transcription of PTS component

132 nella enterica subsp. arizonae This modified V. cholerae strain was able to kill its parent using its

133 the diversity of GIs circulating in natural V. cholerae populations and identifies GIs with VPI-1 re

134 unassociated cases of nonfatal, nontoxigenic V. cholerae non-O1, non-O139 bacteremia in patients with

135 The El Tor and classical biotypes of O1 V. cholerae show striking differences in their resistanc

136 re, suggesting a need to monitor non-O1/O139 V. cholerae in the interest of public health.

137 additional virulence factors in non-O1/O139 V. cholerae yet to be determined.

138 ave been pivotal in the evolution of O1/O139 V. cholerae.

139 phosphoethanolamine (pEtN) to the lipid A of V. cholerae El Tor that is not functional in the classic

140 heme-independent mechanism for activation of V. cholerae H-NOX that implicates this protein as a dual

141 tiated almost immediately after adherence of V. cholerae to intestinal cells.

142 s observed within 30 minutes of adherence of V. cholerae to the intestinal cell line INT 407, and a m

143 The technique involved an amplification of V. cholerae DNA on the surface of an MPNP and then emplo

144 Comparative analyses of V. cholerae mutants suggest that PBP1a/LpoA of V. choler

145 by specifically binding to the O-antigen of V. cholerae We demonstrate that the bivalent structure o

146 ich is implicated in host cell attachment of V. cholerae, associated normally with host cilia.

147 biofilm communities enhance the capacity of V. cholerae to persist in aquatic environments.

148 hin 29 days after the first report, cases of V. cholerae O1 (serotype Ogawa, biotype El Tor) were con

149 re, we present the first characterization of V. cholerae's 'cluster III' chemotaxis system.

150 found that isolation of pathogenic clones of V. cholerae from surface waters in Bangladesh is dramati

151 This toxigenic conversion of V. cholerae has evident implication in both genome plast

152 nsitive and reliable method for detection of V. cholerae in natural samples.

153 providing a strategy for early detection of V. cholerae in surface waters that have been contaminate

154 However, detection of V. cholerae in water is complicated by the existence of

155 ns, based on lipopolysaccharide detection of V. cholerae O1 or O139, may assist in early outbreak det

156 Direct detection of V. cholerae O139 in various fresh seafood samples could

157 s method with former report for detection of V. cholerae published in 2006.

158 to target in the prevention and dispersal of V. cholerae biofilms.

159 dynamic stability of the effector domains of V. cholerae and A. hydrophila MARTX toxins to elucidate

160 ed against a highly lethal challenge dose of V. cholerae N16961.

161 llenged orogastrically with a lethal dose of V. cholerae.

162 in about long-term survival and evolution of V. cholerae strains within these aquatic environmental r

163 bactericidal nor bacteriostatic, exposure of V. cholerae to 2D6 IgA (or Fab fragments) resulted in a

164 Moreover, exposure of V. cholerae to different environmental cues encountered

165 trated in vivo by heterologous expression of V. cholerae pathway enzymes in a specially engineered Es

166 of the secretory traffic and the fitness of V. cholerae in different ecological niches.

167 gative bacteria essential for the fitness of V. cholerae in its natural environment.

168 While the formation of V. cholerae biofilms has been well studied, little is kn

169 ducted with fragmented target DNA (ftDNA) of V. cholerae using electrochemical impedance spectroscopy

170 onstrate that RpoS is required for growth of V. cholerae on insoluble chitin.

171 The identification of V. cholerae O1 strains in the Haitian environment, which

172 t signal for the virulence gene induction of V. cholerae, induces an increase in the number of detach

173 MS identified all 42 isolates of V. cholerae O1 and O139 and 7 of 9 non-O1/O139 isolates.

174 cholerae mutants suggest that PBP1a/LpoA of V. cholerae play a more prominent role in generating and

175 PNP yielded a sensitivity of 10(3) CFU/mL of V. cholerae in buffer system within 4 h.

176 Therefore, c-di-GMP prevents motility of V. cholerae by two distinct but functionally redundant m

177 ly, c-di-GMP still inhibited the motility of V. cholerae only expressing the c-di-GMP blind FlrA(R176

178 A number of V. cholerae iron acquisition systems have been identifie

179 The lowest number of V. cholerae O1 in food sample with and without the enric

180 S system contributes to the pathogenicity of V. cholerae by secreting proteins such as cholera toxin

181 hitectures that separate the major phases of V. cholerae biofilm growth.

182 olysaccharide and capsular polysaccharide of V. cholerae O139.

183 gnificantly alter the virulence potential of V. cholerae shed from cholera patients.

184 undance also covaried with the prevalence of V. cholerae (P < 0.05), but there was no significant rel

185 igen (a bacterial outer-membrane protein) of V. cholerae was expressed and purified and raising of po

186 stream trisaccharide fragment of the O-PS of V. cholerae O139.

187 tag for the detection and quantification of V. cholerae lolB gene single-stranded asymmetric PCR amp

188 ation interface mutants (N381A and R385A) of V. cholerae DAPDC.

189 determined the minimum competence regulon of V. cholerae, which includes at least 19 genes.

190 ptional analysis of the salinity response of V. cholerae, we identified a transcriptional regulator w

191 DNA (cDNA) isolated from clinical samples of V. cholerae was subjected to DNA hybridization studies u

192 -care (POC) devices for in situ screening of V. cholerae related diseases.

193 nt of antimicrobial resistance and spread of V. cholerae O1 El Tor variants expressing the classical

194 In this work, we examined a rugose strain of V. cholerae and its mutants unable to produce matrix pro

195 nated GIVchS12) from a non-O1/O139 strain of V. cholerae that is present in the same chromosomal loca

196 Both El Tor and classical strains of V. cholerae activated ASC (apoptosis-associated speck-li

197 ing of environmental and clinical strains of V. cholerae are needed to understand determinants of cho

198 wild-type and isogenic DeltarpoE strains of V. cholerae, providing additional support for the idea t

199 re widespread among environmental strains of V. cholerae, suggesting that there might be additional v

200 teins lead to competition between strains of V. cholerae, which are thought to be protected only from

201 sal escape response in pathogenic strains of V. cholerae.

202 ed VolA likely contributes to the success of V. cholerae, improving the overall adaptation and surviv

203 ned AI synthase genes, increased survival of V. cholerae and a decrease in phage titer was observed.

204 -induced lipid wasting to extend survival of V. cholerae-infected flies.

205 pread than and largely distinct from that of V. cholerae, likely due to the distinct ways in which th

206 in the delivery of accessory T6SS toxins of V. cholerae.

207 A is the result of multifactorial effects on V. cholerae, including agglutination, motility arrest, a

208 similar to GIVchS12 were identified in other V. cholerae genomes, also containing CRISPR-Cas elements

209 em is conserved in pandemic and non-pandemic V. cholerae strains.

210 As a waterborne pathogen, V. cholerae moves between two dissimilar environments, a

211 on, are specific to the suspected pathogenic V. cholerae O1 and O139, but they are not specific to th

212 drive the genomic diversity of intra-patient V. cholerae populations.

213 C. elegans prefers V. cholerae that produces CAI-1 over a V. cholerae mutan

214 ctor that directly regulates the two primary V. cholerae virulence factors.

215 e ligated-ileal-loop assay, 2D6 IgA promoted V. cholerae agglutination in the intestinal lumen and li

216 ucin, the major component of mucus, promoted V. cholerae movement on semisolid medium and in liquid m

217 The T6SS not only promotes V. cholerae's survival during its aquatic and host life

218 ecules called autoinducers (AIs) can protect V. cholerae against predatory phages.

219 Mutation of either oxyR2 or ahpC rendered V. cholerae more resistant to H2O2 RNA sequencing analys

220 permidine and spermidine enhance and repress V. cholerae biofilm formation, respectively.

221 intestine retards this process by repressing V. cholerae succinate uptake.

222 ge resistance, and moreover, phage-resistant V. cholerae populations were composed of a heterogeneous

223 n studies, establish that R. obeum restricts V. cholerae colonization, that R. obeum luxS (autoinduce

224 , inactivation of the T2S system in a rugose V. cholerae strain prevented the development of colony c

225 uorum-sensing-mediated repression of several V. cholerae colonization factors.

226 ens included cholera toxin B and A subunits, V. cholerae O-specific polysaccharide and lipopolysaccha

227 None of the surviving V. cholerae colonies are resistant to all three phages.

228 This result also demonstrated that V. cholerae T6SS is capable of delivering effectors that

229 Furthermore, we found that V. cholerae is only able to induce virulence in response

230 Recently, it was found that V. cholerae isolates from the Haiti outbreak were poorly

231 We found that V. cholerae Mlc activates biofilm formation in LB broth

232 clinical relevance was the observation that V. cholerae in the INT 407-associated biofilms was signi

233 Our results lead us to propose that V. cholerae senses distinct microenvironments within the

234 ll, the studies presented here revealed that V. cholerae virulence potential can evolve and that the

235 Here, we show that V. cholerae AmiB is crucial for cell division and growth

236 In the present study, we show that V. cholerae OmpU has the ability to induce target cell d

237 These results suggest that V. cholerae is able to sense mucosal signals and modulat

238 These results suggest that V. cholerae O395 OMVs modulate the epithelial proinflamm

239 extracellular traps (NETs), suggesting that V. cholerae DNases combat NETs.

240 t alter rates of detachment, suggesting that V. cholerae undergoes a passive dispersal.

241 Evidence suggests that V. cholerae O1 may activate inflammatory pathways, and a

242 The V. cholerae strip test provides several advantages over

243 The V. cholerae virulence pathway involves an unusual transc

244 to identify genes that were regulated by the V. cholerae Cpx system.

245 rate a new role in biofilm formation for the V. cholerae T2S system, since wild-type V. cholerae was

246 ication mechanism that only functions in the V. cholerae El Tor biotype.

247 7 predicted endochitinase-like genes in the V. cholerae genome.

248 t OxyR2 and AhpC play important roles in the V. cholerae oxidative stress response.

249 Bicarbonate is taken up into the V. cholerae cell, where it positively affects ToxT activ

250 ortant GI involved in cholera disease is the V. cholerae pathogenicity island 1 (VPI-1).

251 ervations suggest that the activation of the V. cholerae Cpx system does not induce expression of gen

252 gulator FleQ, is the master regulator of the V. cholerae flagellar biosynthesis regulon.

253 Moreover, orthologs of the V. cholerae norspermidine biosynthetic pathway are absen

254 crease the negatively charged surface of the V. cholerae outer membrane.

255 the enzyme I (EI) and Hpr components of the V. cholerae phosphoenolpyruvate phosphotransferase syste

256 culate that the reciprocal regulation of the V. cholerae RND efflux systems and the Cpx two-component

257 of a mechanism for direct activation of the V. cholerae virulence cascade by a host signal molecule.

258 a novel pathway that does not depend on the V. cholerae AI-2 sensor, LuxP.

259 Here, we have expressed and purified the V. cholerae HisKa (HnoK) and H-NOX in its heme-bound (ho

260 n for synthetic lethality, we found that the V. cholerae PBP1a and PBP1b proteins, like their Escheri

261 Our findings reveal that the V. cholerae PTS is an additional modulator of the ToxT r

262 SS locus and VgrG3 gene, suggesting that the V. cholerae T6SS is functional and mediates antagonistic

263 Thus, the V. cholerae T6SS contributes to the competitive behaviou

264 Notably, even though V. cholerae EnvC and NlpD appear to be functionally redu

265 omplex was continuously expressed throughout V. cholerae growth, whereas there was growth phase-depen

266 , this biosensor was successfully applied to V. cholerae detection in environmental samples with no s

267 we demonstrate that heme is not available to V. cholerae in the infant mouse intestine.

268 vel noncoding RNA species that contribute to V. cholerae growth.

269 es the expression of ohrA and contributes to V. cholerae's ability to survive in a variety of environ

270 hundred genes were identified as critical to V. cholerae in vivo fitness.

271 The innate response to V. cholerae deleted for cholera toxin-encoding phage (CT

272 Innate immune responses to V. cholerae are not a major cause of cholera pathology,

273 tility for interrogating innate responses to V. cholerae infection.

274 This phenomenon is not unique to V. cholerae; secreted virulence factors that are depende

275 tal introductions of seventh pandemic El Tor V. cholerae and that at least seven lineages local to th

276 The almEFG operon found in El Tor V. cholerae confers >100-fold resistance to antimicrobia

277 colony-forming units/ml) for both toxigenic V. cholerae serogroups.

278 c environments, with environmental toxigenic V. cholerae O1 strains serving as a source for recurrent

279 e a perennial aquatic reservoir of toxigenic V. cholerae around the continent.

280 cted with low or moderate doses of toxigenic V. cholerae El Tor O1.

281 ideo microscopy analysis of antibody-treated V. cholerae in liquid medium revealed that 2D6 IgA not o

282 ential RNA sequencing (RNA-seq) of wild-type V. cholerae and a locked low-cell-density QS-mutant stra

283 ted approximately 1 x 10(5) CFU of wild-type V. cholerae O1 El Tor Inaba strain N16961 10 days or 3 m

284 By comparing TcpP diffusion in wild-type V. cholerae to that in mutant strains lacking either tox

285 the V. cholerae T2S system, since wild-type V. cholerae was found to secrete the biofilm matrix prot

286 Unlike wild-type V. cholerae, mutants lacking wigR fail to recover follow

287 These effects are relevant for understanding V. cholerae pathogenicity and are mediated through the p

288 barriers to infection and showed unexpected V. cholerae migration counter to intestinal flow.

289 ent increases in its relative abundance upon V. cholerae infection of the mice.

290 Using V. cholerae, E. coli and B. subtilis as models, we discu

291 kling mice from oral challenge with virulent V. cholerae O395.

292 ude that V. parahaemolyticus, V. vulnificus, V. cholerae and subpopulations that harbour genes common

293 Therefore, we questioned whether V. cholerae Mlc functions differently than E. coli Mlc.

294 Thus, we propose a model in which V. cholerae ingested as a biofilm has coopted the host-d

295 Co-colonization with V. cholerae mutants discloses that R. obeum AI-2 reduces

296 Intestinal colonization with V. cholerae results in expenditure of host lipid stores

297 other mechanisms to limit colonization with V. cholerae, or conceivably other enteropathogens.

298 he small intestine of patients infected with V. cholerae O1 to characterize the host response to this

299 AI-2 production increase significantly with V. cholerae invasion, and that R. obeum AI-2 causes quor

300 hway involves the zinc metalloprotease YaeL; V. cholerae cells lacking YaeL accumulate a truncated ye