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 lar pathotype: 13 (14%) were DEC (10 EAEC, 2 EPEC, 1 ETEC) (12 associated with TD) and 39 (41%) ExPEC

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 young children in developing countries, and EPEC isolates can be subdivided into two groups.

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

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

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

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

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

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 imited, and the emerging process of STEC and EPEC is largely unknown.

39 ed, respectively, and revealed that STEC and EPEC strains have emerged in multiple sublineages of the

40 ught to be the primary reservoir of STEC and EPEC.

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

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

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

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

45 Atypical EPEC (aEPEC) bacteria also contain the LEE but lack the

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

47 s have been historically designated atypical EPEC.

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

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

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

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

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

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

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

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

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

57 mplex regulating actin pedestal formation by EPEC.

58 modulin modulate actin pedestal formation by EPEC.

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

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

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

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

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

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

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

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

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

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

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

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

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

72 ia coli (STEC) and enteropathogenic E. coli (EPEC) are the major foodborne pathogens that can cause h

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

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

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

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

77 to be mistyped as enteropathogenic E. coli (EPEC) or enterohemorrhagic E. coli (EHEC) owing to share

78 ved in EHEC and in enteropathogenic E. coli (EPEC) strains.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

113 Enteropathogenic Escherichia coli (EPEC) is a leading cause of moderate to severe diarrhea

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

131 ng of the enteropathogenic Escherichia coli (EPEC) type III secretion system (T3SS) effector transloc

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

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

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

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

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

137 effacing enteropathogenic Escherichia coli (EPEC).

138 nicity of enteropathogenic Escherichia coli (EPEC).

139 model for enteropathogenic Escherichia coli (EPEC).

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

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

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

143 ve E. coli [EAEC], enteropathogenic E. coli [EPEC], enterotoxigenic E. coli [ETEC], enteroinvasive E.

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

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

146 y needed to develop new strategies to combat EPEC.

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

148 al that of its better-characterized cousins, EPEC and EHEC.

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

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

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

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

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

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

155 is a key proximal signaling molecule during EPEC pathogenesis.

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

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

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

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

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

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

162 Furthermore, EPEC infection inhibits TNF-induced phosphorylation and

163 confirmed the key regulatory role of Ca2+ in EPEC-induced pyroptosis.

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

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

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

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

168 STEC strains that parallel those observed in EPEC.

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

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

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

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

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

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

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

176 an commensal and clinical strains, including EPEC and STEC, at a global level.

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

178 r chelation of extracellular Ca2+, inhibited EPEC-induced cell death.

179 was common (24.2%), most commonly involving EPEC, EAEC, ETEC, and STEC.

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

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

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

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

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

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

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

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

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

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

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

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

192 (T3SS) is the major virulence determinant of EPEC and is also possessed by major STEC lineages.

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

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

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

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

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

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

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

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

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

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

203 expression contributes to the maintenance of EPEC colonization.

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 (ECP) to the overall adherence properties of EPEC.

210 ferences in the global virulence regulons of EPEC isolates.

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

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

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

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

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

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

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

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

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

220 effect of Tir clustering on the viability of EPEC-infected intestinal epithelial cells (IECs) is unkn

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

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

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

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

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

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

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

228 reports demonstrating that many provisional EPEC and EHEC isolates incriminated in disease outbreaks

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

246 We show that EPEC induces pyroptosis in IECs in a Tir-dependent but a

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

266 These EPEC isolates exhibited previously unappreciated phyloge

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

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

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

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

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

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

273 e attaching and effacing pathogen related to EPEC.

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

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

276 duced polymerization of actin in response to EPEC.

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

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

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

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

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

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

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

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

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

286 Typical EPEC (tEPEC) bacteria are characterized by the presence

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

288 Typical EPEC infection is rare in animals and poorly reproduced

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

290 la, Salmonella, ETEC, sapovirus, and typical EPEC.

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.