ライフサイエンスコーパス: EPEC

1 EPEC also disrupts epithelial barrier function and cause

2 EPEC and EHEC not only induce characteristic attaching a

3 EPEC attaches to the apical surface of small intestine e

4 EPEC induced PepT1 expression and activity in HT29-Cl.19

5 EPEC induced the autophosphorylation of EGFR in intestin

6 EPEC infection (60 minutes-3 hours) inhibited apical Cl(

7 EPEC infection decreased V(max) of the transporter; wher

8 EPEC infection in vivo (1 day) also caused marked redist

9 EPEC infection inhibits RNase L in a T3SS-dependent mann

10 EPEC infection of mice (24 hours) reduced SERT immunosta

11 EPEC is a human-specific pathogen whose pathogenesis can

12 EPEC modulates host cell survival and inflammation, alth

13 EPEC pathogenesis occurs through type III secretion syst

14 EPEC pathogenesis relies on a type III secretion system-

15 EPEC translocates effector molecules into host cells via

16 EPEC was also able to inject effectors into DCs sending

17 EPEC-induced EGFR phosphorylation was blocked by the pha

18 EPEC-mediated Akt phosphorylation, however, was inhibite

19 ted diarrhea (RR, 0.41 [95% CI, 0.16-1.00]), EPEC-associated fever (RR, 0.15 [95% CI, 0.02-0.98]), an

20 roups, including enteropathogenic E. coli 2 (EPEC 2), enterohemorrhagic E. coli 2 (EHEC 2), and EHEC-

21 after a 20-h infection and protected against EPEC-induced histologic damage.

22 We therefore established an EPEC infection model in human gut xenografts in SCID mic

23 ound that the BFP biogenesis machine from an EPEC strain that expresses one bundlin type is capable o

24 intestinal epithelial cells infected with an EPEC espZ mutant (DeltaespZ) showed increased levels of

25 Interestingly, infection of cells with an EPEC mutant deficient in espG significantly attenuated t

26 6 strain E2348/69 (United Kingdom, 1969) and EPEC O55:H7 strain CB9615 (Germany, 2003).

27 the present study, we investigated CD98 and EPEC interactions in vitro and ex vivo and examined FVB

28 viously reported that the conserved EHEC and EPEC effector EspG disrupts recycling endosome function,

29 A genetic approach showed that EHEC and EPEC fliC deletion mutants were significantly less adher

30 We show that the EHEC and EPEC NleH effectors are functionally equivalent in their

31 enteropathogenic Escherichia coli (EHEC and EPEC), as well as the related mouse pathogen Citrobacter

32 as a model of human intestinal epithelia and EPEC-infected C57BL/6J mouse model of infection were uti

33 individuals who are coinfected with ETEC and EPEC.

34 ffer between EHEC O157:H7, EHEC O26:H11, and EPEC O127:H6 in terms of the number of SH3-binding polyp

35 d the abilities of EHEC EDL933 (O157:H7) and EPEC E2348/69 (O127:H6) flagella to bind to bovine mucus

36 direct binding between recombinant hCD98 and EPEC/C. rodentium proteins.

37 Our analysis suggests that C. rodentium and EPEC/EHEC have converged on a common host infection stra

38 MN transepithelial migration in Shigella and EPEC infections.

39 Therefore, ETEC toxins and EPEC-induced damage to the host cell both enhance the vi

40 are normally recruited by vaccinia virus and EPEC in the absence of WIP, and neither WIP nor the WIP

41 emphasizes the zoonotic potential of animal EPEC strains and the need for virulence determinant-base

42 mmune response to enteric pathogens, such as EPEC, and its impact on IEC barrier function have not be

43 lysis identified a single disease-associated EPEC O145:H2 strain.

44 In contrast, atypical EPEC (aEPEC) infection is common in both children and an

45 s have been historically designated atypical EPEC.

46 enteropathogenic E. coli (EPEC), or atypical EPEC, depending on the presence or absence of the Shiga

47 r facilities and determined to shed atypical EPEC at a culture-based prevalence of 18%.

48 ncreased severity of illness, while atypical EPEC lack this feature.

49 Tec-family tyrosine kinases localize beneath EPEC and, with Abl-family kinases, comprise a set of red

50 factors, such as bundle-forming pilus (BFP), EPEC secreted protein A, and other EPEC secreted protein

51 In addition, although Nck binds EPEC Tir directly, N-WASP is required for its localizati

52 Both EPEC and S. flexneri rely on type three secretion system

53 lates that contain virulence factors of both EPEC and ETEC.

54 Induction of PepT1 expression by EPEC required the transcription factor Cdx2.

55 mplex regulating actin pedestal formation by EPEC.

56 modulin modulate actin pedestal formation by EPEC.

57 ortant for the inhibition of phagocytosis by EPEC and also limits EPEC translocation through antigen-

58 or cycle inhibiting factor (Cif) produced by EPEC and EHEC is able to block host eukaryotic cell-cycl

59 ur results demonstrate inhibition of SERT by EPEC and define the mechanisms underlying these effects.

60 ight similar pathogenic strategies shared by EPEC and vaccinia virus by demonstrating a requirement f

61 n IEC barrier functions that are targeted by EPEC effectors to escape host defense mechanisms and pro

62 a set of redundant host kinases utilized by EPEC to form actin pedestals.

63 n attachment to intestinal epithelial cells, EPEC induces actin-filled membrane protrusions called 'p

64 Screening a collection of clinical EPEC isolates revealed that espW is present in 52% of th

65 ing/effacing (A/E) human pathogenic E. coli (EPEC and EHEC) and the natural mouse pathogen Citrobacte

66 an disease are the enteropathogenic E. coli (EPEC) and enterotoxigenic E. coli (ETEC).

67 ctions in EHEC and enteropathogenic E. coli (EPEC) and found that five interactions were conserved.

68 ia coli (ETEC) and enteropathogenic E. coli (EPEC) are common causes of diarrhea in children in devel

69 ia coli (EHEC) and enteropathogenic E. coli (EPEC) are enteric bacterial pathogens of worldwide impor

70 g E. coli; whereas enteropathogenic E. coli (EPEC) are LEE+ and often carry the EPEC adherence factor

71 Enteropathogenic E. coli (EPEC) is a human pathogen that targets the small intesti

72 Enteropathogenic E. coli (EPEC) is a major cause of infantile diarrhea, but the pa

73 disease caused by enteropathogenic E. coli (EPEC) is dependent on a delivery system that injects num

74 from its ancestor, enteropathogenic E. coli (EPEC) O55:H7 (sorbitol fermenting [SOR(+)] and beta-gluc

75 t the adherence of enteropathogenic E. coli (EPEC) to epithelial monolayers, and (4) limit bacterial

76 pic variability in enteropathogenic E. coli (EPEC), an important human pathogen, both in virulence ac

77 ichia coli (EHEC), enteropathogenic E. coli (EPEC), and Citrobacter rodentium Moreover, Salmonella en

78 li (EHEC), typical enteropathogenic E. coli (EPEC), or atypical EPEC, depending on the presence or ab

79 ic E. coli (ETEC), enteropathogenic E. coli (EPEC), Shigella spp., Campylobacter jejuni, Salmonella e

80 richia coli (ETEC), enteropathogenic E.coli (EPEC), Listeria monocytogenes, Salmonella entericaserova

81 enic and enterohemorrhagic Escherichia coli (EPEC and EHEC) functions to activate transcription of vi

82 enic and enterohemorrhagic Escherichia coli (EPEC and EHEC) share a unique mechanism of colonization

83 enic and enterohemorrhagic Escherichia coli (EPEC and EHEC) use a type III protein secretion system (

84 enic and enterohemorrhagic Escherichia coli (EPEC and EHEC, respectively), C. rodentium exploits a ty

85 enic and enterohemorrhagic Escherichia coli (EPEC and EHEC, respectively), which inhibit Src kinase-d

86 enic and enterohemorrhagic Escherichia coli (EPEC and EHEC, respectively).

87 enic and enterohemorrhagic Escherichia coli (EPEC and EHEC, respectively).

88 s such as enteropathogenic Escherichia coli (EPEC) and Citrobacter rodentium during mammalian infecti

89 agella of enteropathogenic Escherichia coli (EPEC) and enterohemorrhagic E. coli (EHEC) might contrib

90 pathogens enteropathogenic Escherichia coli (EPEC) and enterohemorrhagic E. coli employ a type 3 secr

91 actors in enteropathogenic Escherichia coli (EPEC) and reduced EPEC-induced intestinal damage in vivo

92 tion with enteropathogenic Escherichia coli (EPEC) and Shiga-toxigenic E. coli (STEC), also known as

93 Enteropathogenic Escherichia coli (EPEC) and Shigella flexneri are human host-specific path

94 pathogens enteropathogenic Escherichia coli (EPEC) and vaccinia virus trigger actin assembly in host

95 he world, enteropathogenic Escherichia coli (EPEC) are a leading cause of death in children with diar

96 Enteropathogenic Escherichia coli (EPEC) are diarrhoeagenic E. coli, and are a significant

97 sented in enteropathogenic Escherichia coli (EPEC) by EspB and EspD, which are thought to interact an

98 Enteropathogenic Escherichia coli (EPEC) cause intestinal inflammation, severe diarrhoea an

99 ninvasive enteropathogenic Escherichia coli (EPEC) colonize the gut using a type three secretion syst

100 Enteropathogenic Escherichia coli (EPEC) continues to be a leading cause of mortality and m

101 pathogen enteropathogenic Escherichia coli (EPEC) forms characteristic actin-filled membranous protr

102 lmarks of enteropathogenic Escherichia coli (EPEC) infection are formation of attaching and effacing

103 llmark of enteropathogenic Escherichia coli (EPEC) infection is the formation of actin-rich pedestal-

104 Enteropathogenic Escherichia coli (EPEC) infection triggers the release of ATP from host in

105 Enteropathogenic Escherichia coli (EPEC) inhibits inflammation by an undefined, T3SS-depend

106 nfection, enteropathogenic Escherichia coli (EPEC) injects effector proteins into the host cell to ma

107 , typical enteropathogenic Escherichia coli (EPEC) is a common cause of diarrhea and is associated wi

108 Enteropathogenic Escherichia coli (EPEC) is a food-borne human pathogen that attaches to IE

109 Enteropathogenic Escherichia coli (EPEC) is a leading cause of severe intestinal disease an

110 Enteropathogenic Escherichia coli (EPEC) is a major cause of diarrheal disease in young chi

111 (BFP) of enteropathogenic Escherichia coli (EPEC) is a prototypical T4P and confirmed virulence fact

112 Enteropathogenic Escherichia coli (EPEC) is an important cause of infantile diarrhea, espec

113 (BFP) of enteropathogenic Escherichia coli (EPEC) is an important virulence factor.

114 pathogen enteropathogenic Escherichia coli (EPEC) is not known.

115 pathogen enteropathogenic Escherichia coli (EPEC) is responsible for significant infant mortality an

116 Enteropathogenic Escherichia coli (EPEC) is the most important cause of persistent diarrhea

117 Enteropathogenic Escherichia coli (EPEC) is the single most important contributor to child

118 t, and in enteropathogenic Escherichia coli (EPEC) it is mediated by several adhesins, including the

119 pathogen enteropathogenic Escherichia coli (EPEC) limits the death of infected enterocytes early in

120 The enteropathogenic Escherichia coli (EPEC) locus of enterocyte effacement (LEE)-encoded effec

121 (BFP) of enteropathogenic Escherichia coli (EPEC) mediates microcolony formation on epithelial cells

122 osed with enteropathogenic Escherichia coli (EPEC) on the basis of postmortem light microscopic and,

123 Enteropathogenic Escherichia coli (EPEC) primarily infects children in developing countries

124 ce of the enteropathogenic Escherichia coli (EPEC) serotype is of particular concern, as this group o

125 athogens, enteropathogenic Escherichia coli (EPEC) stands out as showing the highest risk for infecti

126 n O119:H2 enteropathogenic Escherichia coli (EPEC) strain MB80 by subtractive hybridization is encode

127 Enteropathogenic Escherichia coli (EPEC) strains continue to cause severe and sometimes fat

128 that the enteropathogenic Escherichia coli (EPEC) type III effector protein EspF nucleates a multipr

129 Enteropathogenic Escherichia coli (EPEC) use a type III secretion system (T3SS) to alter ho

130 pathogen enteropathogenic Escherichia coli (EPEC) uses the type III secretion system (T3SS) effector

131 Enteropathogenic Escherichia coli (EPEC), a major cause of watery diarrhea in infants and a

132 llmark of enteropathogenic Escherichia coli (EPEC), enterohemorrhagic E. coli (EHEC) and Citrobacter

133 eened for enteropathogenic Escherichia coli (EPEC), enterotoxigenic E. coli (ETEC), Shiga toxin-produ

134 tility of enteropathogenic Escherichia coli (EPEC), vaccinia, and other vertebrate poxviruses by inte

135 effacing enteropathogenic Escherichia coli (EPEC).

136 nicity of enteropathogenic Escherichia coli (EPEC).

137 model for enteropathogenic Escherichia coli (EPEC).

138 anel were enteropathogenic Escherichia coli (EPEC, n = 21), norovirus (n = 21), rotavirus (n = 15), s

139 nic and enterohaemorrhagic Escherichia coli (EPEC/EHEC) manipulate a plethora of host cell processes

140 ic E. coli [ETEC], enteropathogenic E. coli [EPEC], and Shiga-toxigenic E. coli [STEC]), Shigella/ent

141 e host and enteropathogenic Escherichia coli(EPEC) and Shiga-toxigenic E. coli(STEC).

142 Enteropathogenic Escherichia coli(EPEC) requires the tnaA-encoded enzyme tryptophanase and

143 y needed to develop new strategies to combat EPEC.

144 In conclusion, EPEC, through the T3SS-dependent translocation of NleF,

145 This study confirms EPEC's potential for dissemination of virulence attribut

146 ition of EGFR phosphorylation also curtailed EPEC-induced ERK1/2 (MAP kinase) phosphorylation and, co

147 The best-described EPEC effectors are encoded together on the locus of ente

148 ce plasmid, distinct from the well-described EPEC adherence factor (EAF) plasmid.

149 L-8) following ectopic expression and during EPEC infection.

150 However, NleB delivery during EPEC and C. rodentium infection caused rapid and prefere

151 o visualize uric acid crystals formed during EPEC and STEC infections, we noticed that uric acid crys

152 is a key proximal signaling molecule during EPEC pathogenesis.

153 XO released during EPEC and STEC infection may serve as a virulence-inducin

154 and we previously identified enteroadherent EPEC in the intestines of deceased kittens.

155 In this report, enzootic EPEC infection associated with up to 10.5% diarrhea-asso

156 n to dampen host inflammation and facilitate EPEC colonization during pathogenesis.

157 Following EPEC O127:H6 strain E2348/69 infection, T3SS-dependent A

158 we report that IFN-beta is induced following EPEC infection and regulates IEC TJ proteins to maintain

159 Nevertheless, the mechanism responsible for EPEC diarrhoea remains elusive.

160 Furthermore, EPEC infection inhibits TNF-induced phosphorylation and

161 examined the role of the host enzyme CD73 in EPEC infection by testing the effect of ecto-5'-nucleoti

162 ed to investigate the genomic differences in EPEC isolates obtained from individuals with various cli

163 XO is released into intestinal fluids in EPEC and STEC infection in a rabbit animal model.

164 n, and luciferase expression was measured in EPEC-infected mice by bioluminescence using an in vivo i

165 STEC strains that parallel those observed in EPEC.

166 . rodentium-specific (without orthologues in EPEC or EHEC) coding sequences, 10 prophage-like regions

167 aining the first 206 residues, is present in EPEC strains belonging to serotype O55:H7.

168 es that were significantly more prevalent in EPEC isolates of symptomatic and lethal outcomes than in

169 nal membrane Cl(-)/OH(-) exchange process in EPEC pathogenesis using in vitro and in vivo models.

170 ele, encoding an uncleavable LexA protein in EPEC, resulted in reduced secretion, particularly in the

171 er DRA (SLC26A3) was considerably reduced in EPEC-infected cells, corresponding with decreased Cl(-)/

172 s of symptomatic and lethal outcomes than in EPEC isolates of asymptomatic outcomes.

173 arguing against an essential role for WIP in EPEC-induced actin assembly.

174 e pattern, as seen in diarrheic human infant EPEC isolates.

175 tion of phagocytosis by EPEC and also limits EPEC translocation through antigen-sampling cells (M cel

176 sponses after an initial challenge with live EPEC were stronger against the homologous bundlin protei

177 y be one of the factors required to maintain EPEC colonization.

178 Most EPEC and non-O157 EHEC strains express lymphostatin (als

179 When cultured with a mutant EPEC unable to translocate effector proteins, myeloid DC

180 SseK1, SseK3, EHEC NleB1, EPEC NleB1, and Crodentium NleB blocked TNF-mediated NF-

181 C. rodentium NleB, EHEC NleB1, EPEC NleB1, and SseK2 glycosylated the FADD (Fas-associa

182 cylation during ectopic expression of NleB1, EPEC infection in vitro, or C. rodentium infection in vi

183 ants, however, did not affect the ability of EPEC to form actin pedestals, arguing against an essenti

184 -BBE cells showed a decrease in adherence of EPEC to Caco2 cells in which CD98 expression was knocked

185 bbit ileal loops, decreased the adherence of EPEC to rabbit ileum, and reduced histopathological dama

186 eat deal to learn about the genetic basis of EPEC virulence.

187 PepT1 expression reduced binding of EPEC to lipid rafts, as well as activation of nuclear fa

188 aching and effacing effect characteristic of EPEC and enterohemorrhagic E. coli and has been posited

189 inhibits actin polymerization downstream of EPEC, Vaccinia virus and opsonized red blood cells.

190 n A supplementation had shorter durations of EPEC-associated diarrhea than did children who did not r

191 We therefore examined the effect of EPEC on the epidermal growth factor receptor (EGFR), a k

192 odentium are all 22 of the core effectors of EPEC strain E2348/69.

193 The present studies examined the effects of EPEC infection on SERT activity and expression in intest

194 esized that the anti-inflammatory effects of EPEC were mediated by NleH1 and NleH2.

195 produced and that the T3SS effector EspB of EPEC, and heat-labile toxin of ETEC were secreted.

196 owth, caused a decrease in the expression of EPEC protein virulence factors, such as bundle-forming p

197 EspB, a key virulence factor of EPEC, is required for the attaching and effacing effect

198 A defining feature of EPEC disease is the loss (effacement) of absorptive micr

199 ons that produced little or no inhibition of EPEC growth, caused a decrease in the expression of EPEC

200 to the multifactorial complex interaction of EPEC with host epithelial cells.

201 expression contributes to the maintenance of EPEC colonization.

202 provide new insights into the mechanisms of EPEC diarrhoea.

203 ing the Citrobacter rodentium mouse model of EPEC.

204 An nleE deletion mutant of EPEC showed a similar reduction of PMN migration.

205 , addition of DNase I reduced the numbers of EPEC bacteria recovered after a 20-h infection and prote

206 ch of what we know about the pathogenesis of EPEC infections is based on the study of one or two prot

207 s into the epidemiology and pathogenicity of EPEC by enabling the detection and tracking of specific

208 apable of directly detecting the presence of EPEC within 5 min, has been developed using a simple mic

209 pplementation also reduced the prevalence of EPEC-associated diarrhea (RR, 0.41 [95% CI, 0.16-1.00]),

210 (ECP) to the overall adherence properties of EPEC.

211 ferences in the global virulence regulons of EPEC isolates.

212 cum is not only a major colonization site of EPEC but also a site of EPEC effector gene expression in

213 colonization site of EPEC but also a site of EPEC effector gene expression in mice.

214 eins co-localize with the infection sites of EPEC.

215 , and our data might explain how a subset of EPEC effector proteins, encoded in cryptic prophages, ar

216 Filter-sterilized supernatants of EPEC cultures also stimulated EGFR phosphorylation, sugg

217 hways contribute to the enhanced survival of EPEC-infected host cells.

218 genomes have been fully sequenced: those of EPEC O127:H6 strain E2348/69 (United Kingdom, 1969) and

219 was to determine the prevalence and type of EPEC in kittens and whether infection was associated wit

220 Much of our understanding of EPEC pathogenesis is derived from studies using cell lin

221 lls and also has growth-promoting effects on EPEC bacteria.

222 pear to be due to the action of the metal on EPEC bacteria as well as on the host.

223 Some of the beneficial effects of zinc on EPEC infection appear to be due to the action of the met

224 actin recruitment to sites of attachment, or EPEC-induced epithelial barrier function alteration.

225 us (BFP), EPEC secreted protein A, and other EPEC secreted proteins, and reduced EPEC adherence to ce

226 resistance plasmid were identified in other EPEC strains, including the prototypical O111:NM strain

227 nfection strategy of extracellular pathogens EPEC and EHEC and shed light on the complexities of the

228 zinc was much more efficacious in preventing EPEC-induced fluid secretion in rabbit ileal loops than

229 el form of signaling mimicry used to promote EPEC pathogenesis and gastrointestinal disease.

230 Rabbit EPEC strains were selected for acquisition of Stx-encodi

231 In sampled rabbits, EPEC-positive culture and the presence of diarrhea were

232 However, genomic analysis of recent EPEC isolates has revealed that the EPEC pathotype is mo

233 nd other EPEC secreted proteins, and reduced EPEC adherence to cells in tissue culture.

234 thogenic Escherichia coli (EPEC) and reduced EPEC-induced intestinal damage in vivo.

235 In vivo, zinc reduced EPEC-induced fluid secretion into ligated rabbit ileal l

236 or chelation of intracellular Ca(2+) reduces EPEC-dependent actin polymerization.

237 nal evolution of O157:H7, we fully sequenced EPEC O55:H7 strain RM12579 (California, 1974), which was

238 ight be central mechanisms underlying severe EPEC-mediated disease.

239 Since EPEC is genetically related to Shiga-toxigenic E. coli (

240 s, and compelling evidence for cross-species EPEC transmission exists.

241 dard culture methods detected Shigella spp., EPEC, ETEC, and EAEC in smaller proportions of the sampl

242 days postinfection, when map is suppressed, EPEC colonization is significantly reduced, indicating t

243 In addition, we found that EPEC bacteria and H6 flagella, but not EHEC, bound large

244 Furthermore, we found that EPEC strains expressing divergent bundlin types are capa

245 We hypothesized that EPEC might also inject proteins into DC processes to dam

246 Previously, it has been reported that EPEC, in a T3SS-dependent manner, induces an early proin

247 ce energy transfer-based system we show that EPEC injects effectors into in vitro grown human myeloid

248 Confocal microscopic studies showed that EPEC infection caused a marked redistribution of DRA fro

249 The EPEC T3SS effector NleD counteracts this protective acti

250 locus of enterocyte effacement (LEE) and the EPEC adherence factor (EAF) plasmid.

251 Effacement activity caused by the EPEC protein Map in the Caco-2 but not ex vivo model, wa

252 es to persistent colonization of mice by the EPEC-like mouse pathogen Citrobacter rodentium.

253 E. coli (EPEC) are LEE+ and often carry the EPEC adherence factor plasmid-encoded bundle-forming pil

254 Investigation of the EPEC adherence factor (EAF) plasmids, which carry the BF

255 The recent completion of the EPEC genome sequence suggests its effector repertoire co

256 Two proteins encoded outside of the EPEC locus of enterocyte effacement (LEE) pathogenicity

257 ic framework for aEPEC in the context of the EPEC pathotype and will facilitate further studies into

258 MV effacement activity of the EPEC protein EspF in the TC-7 model was dependent on its

259 Global transcriptional analyses of the EPEC prototype isolate E2348/69 and two EAF plasmid muta

260 , we compared the virulence functions of the EPEC T3SS effector NleE and the homologous Shigella prot

261 r targeting the BfpB secretin protein of the EPEC T4P to the OM and describe the ultrastructure of th

262 e pathogen, as well as the complexity of the EPEC virulence factor repertoire.

263 using RNA sequencing, demonstrated that the EPEC and ETEC virulence genes of these hybrid isolates w

264 f recent EPEC isolates has revealed that the EPEC pathotype is more diverse than previously appreciat

265 Here we report that the EPEC type-III secretion system effector EspJ inhibits au

266 ucosal surfaces following infection with the EPEC-like mouse pathogen Citrobacter rodentium.

267 These EPEC isolates exhibited previously unappreciated phyloge

268 Thus, EPEC translocate effectors into human DCs to dampen the

269 Tir(EPEC/CR) also contains an Asn-Pro-Tyr (NPY(454/1)) motif

270 Phosphorylation of Tir(EPEC/CR) Y474/1 leads to recruitment of Nck and neural W

271 f hCD98 was sufficient for direct binding to EPEC/C. rodentium.

272 G2 play an important role in contributing to EPEC infection-associated inhibition of luminal membrane

273 rid isolates are more genomically-related to EPEC, but appear to have acquired ETEC virulence genes.

274 e attaching and effacing pathogen related to EPEC.

275 IECs upregulate LV production in response to EPEC and other Gram-negative pathogens.

276 vivo in the lumen of the gut in response to EPEC and STEC infections.

277 duced polymerization of actin in response to EPEC.

278 entium Our murine infant model is similar to EPEC infection in human infants since infant mice are mu

279 secreted effector protein that is unique to EPEC and related "attaching and effacing" (A/E) pathogen

280 Comparative genomics of 70 total EPEC from lethal (LI), non-lethal symptomatic (NSI) or a

281 Two EPEC genomes have been fully sequenced: those of EPEC O1

282 ns belonging to this evolutionary model: two EPEC O55:H7 (SOR(+) GUD(+)) strains, two nonmotile EHEC

283 al microbiotas, and anaerobes, but wild-type EPEC and STEC strains were 100 to 1,000 times more resis

284 n of CD80, CD83, and CD86, whereas wild-type EPEC barely elicits cytokine production and shuts off nu

285 DCs cocultured with wild-type EPEC or NleE-complemented strains were less potent at in

286 in as compared with treatment with wild-type EPEC.

287 Typical EPEC are identified by the presence of the bundle-formin

288 Typical EPEC infection is rare in animals and poorly reproduced

289 Typical EPEC isolates are differentiated from other types of pat

290 erize enterohaemorrhagic E. coli and typical EPEC, respectively.

291 In only two kittens was EPEC infection confirmed.

292 insight into the precise mechanisms by which EPEC colonizes the intestine, evades host immunity, and

293 ndent manner, providing a mechanism by which EPEC evades IFN-induced antibacterial activities.

294 Infection of Caco-2 cells with EPEC for 30-120 minutes decreased apical SERT activity (

295 at shares important functional features with EPEC, colonizes mice in colon and cecum and causes infla

296 Infection with EPEC promotes both the interaction of IQGAP1 with calmod

297 experimental model of infant infection with EPEC, using the mouse-specific pathogen Citrobacter rode

298 eltanleH1H2 was cleared more rapidly than WT EPEC while complementation of DeltanleH1H2 with either N

299 ith DeltanleH1H2 than those infected with WT EPEC, indicating that NleH1/H2 dampen pro-inflammatory c

300 in-infected cells compared to wild-type (WT) EPEC-infected cells.