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1 ETEC adheres to host epithelial cells in the small intes
2 ETEC adhesion is mediated by lectins (adhesins) that bin
3 ETEC causes disease by colonizing the small intestine an
4 ETEC infection also caused a drastic inhibition of host
5 ETEC seedlings revealed increased photosynthesis and imp
6 ETEC strains expressing F4 fimbriae are associated with
7 ETEC strains that express the heat-stable toxin (ST), wi
8 ETEC was significantly associated with diarrhea (crude o
9 ETEC-associated diarrhea remains common among children l
10 ETEC-mediated diarrhea is orchestrated by heat-labile to
11 as defined by the reference method was 1.2% ETEC, 0.1% Vibrio, 0% Y. enterocolitica, and 0% P. shige
14 ts showed that high pup survival rates after ETEC challenge were associated with suckling but not bir
18 ies conferred significant protection against ETEC, providing the first clinical evidence that fimbria
20 subunit and live-attenuated vaccines against ETEC and other enteric pathogens, including Shigella fle
24 a heavy chain-only antibodies (VHHs) against ETEC to the Fc part of a porcine immunoglobulin (IgG or
25 ic regions were conserved exclusively in all ETEC genomes; however, we identified more genomic conten
26 ntified more genomic content conserved among ETEC genomes than among non-ETEC E. coli genomes, sugges
30 sites in the genome of H10407 (O78:H11), an ETEC strain that was originally isolated from the stool
35 trobacter rodentium, Salmonella enterica and ETEC were capable of complementing Aar activity by repre
36 A sequencing, demonstrated that the EPEC and ETEC virulence genes of these hybrid isolates were diffe
38 association between H. pylori infection and ETEC diarrhea was similar, albeit not statistically sign
39 As a proof of principle, we designed anti-ETEC antibodies by fusing variable domains of llama heav
42 in complex and dynamic interactions between ETEC and the gastrointestinal mucosae in which host glyc
43 were accompanied by visible changes in both ETEC architecture and the expression of surface antigens
44 ls in a 24 h period) in which either or both ETEC enterotoxins (LT and heat-stable toxin [ST]) were d
45 ying that each fimbrial type was acquired by ETEC strains very recently, consistent with a recent ori
46 compound for treatment of diarrhea caused by ETEC and other adenylyl cyclase toxin-producing bacteria
52 , potentially, secretory outcomes induced by ETEC strains expressing LT+ST compared with strains that
53 host interactions are finely orchestrated by ETEC and are characterized by coordinated responses invo
54 identified a number of molecules produced by ETEC that contribute to its virulence and are novel anti
61 o sequenced a human enterotoxigenic E. coli (ETEC) strain of the same ST23 serogroup O78 lineage.
62 richia coli (EAEC), enterotoxigenic E. coli (ETEC), enteropathogenic E. coli (EPEC), Shigella spp., C
65 (n = 66), enterotoxigenic Escherichia coli (ETEC) (n = 31) or negative for bacterial pathogens (n =
67 termine if enterotoxigenic Escherichia coli (ETEC) and enteroaggregative E. coli (EAEC) DNA could be
69 es against enterotoxigenic Escherichia coli (ETEC) are being developed, many of which target common f
76 imbriae of enterotoxigenic Escherichia coli (ETEC) comprise eight serologically discrete colonization
77 Porcine enterotoxigenic Escherichia coli (ETEC) continues to result in major morbidity and mortali
79 enges with enterotoxigenic Escherichia coli (ETEC) have broadened our understanding of this important
80 antage for enterotoxigenic Escherichia coli (ETEC) in vivo, we hypothesized that LT preconditions the
81 and severe enterotoxigenic Escherichia coli (ETEC) infections are caused by strains that express K88
86 Globally, enterotoxigenic Escherichia coli (ETEC) is a leading cause of childhood and travelers' dia
108 strain of enterotoxigenic Escherichia coli (ETEC) that utilizes CFA/I pili to adhere to surfaces of
111 including enterotoxigenic Escherichia coli (ETEC), a major cause of diarrhoea in travellers and chil
113 disease by enterotoxigenic Escherichia coli (ETEC), an E. coli pathotype that inflicts an enormous gl
115 olerae O1, enterotoxigenic Escherichia coli (ETEC), enteropathogenic E. coli, Campylobacter jejuni, a
116 r included enterotoxigenic Escherichia coli (ETEC), enteropathogenic E.coli (EPEC), Listeria monocyto
117 including enterotoxigenic Escherichia coli (ETEC), produce one or more serine proteases that are sec
118 es against enterotoxigenic Escherichia coli (ETEC), the most common bacteria causing diarrhea in chil
119 ocolitica, enterotoxigenic Escherichia coli (ETEC), Vibrio, and Plesiomonas shigelloides The study in
122 ive E. coli [EAEC], enterotoxigenic E. coli [ETEC], enteropathogenic E. coli [EPEC], and Shiga-toxige
123 ella spp., enterotoxigenic Escherichia coli [ETEC], Shiga toxin-producing E. coli [STEC], E. coli O15
125 onpermeabilized bacteria, while, conversely, ETEC 1766a seems to secrete most of the produced autotra
130 i O148 is a nonencapsulated enterotoxigenic (ETEC) Gram negative bacterium that can cause diarrhea, h
131 nia spp., Citrobacter spp., enterotoxigenic (ETEC) and enteroaggregative E. coli (EAEC), and members
132 ulture methods detected Shigella spp., EPEC, ETEC, and EAEC in smaller proportions of the samples tha
133 itial exposure, only ST and LT/ST-expressing ETEC isolates (P < 0.0001) were associated with disease
134 ntributor than STb to the virulence of F4(+) ETEC infections in young F4ac receptor-positive pigs les
137 dress this, we sequenced the genomes of five ETEC isolates obtained from children in Guinea-Bissau wi
138 f host phosphatidylserine exposure following ETEC infection suggested that ETEC induced changes in pl
139 for all specimens combined were as follows: ETEC, 97.6% (87.4 to 99.6), 99.8% (99.5 to 99.9), and 0.
140 li O157:H7; 95% for Giardia lamblia; 94% for ETEC and STEC; 93% for Shigella spp.; 92% for Salmonella
142 ith alternate PCR and sequencing, except for ETEC, for which the reference method was two alternate P
143 l molecular signaling events responsible for ETEC-induced diarrhea, including cyclic GMP (cGMP) produ
144 five E. coli-like colonies were screened for ETEC enterotoxins using a GM1 enzyme-linked immunosorben
145 he availability of genomic DNA sequences for ETEC strains coupled with proteomics technology affords
149 containing heat-labile enterotoxin (LT) from ETEC delivered to the skin by patch in travellers to Mex
152 in addition to the two previously generated ETEC genomes, highlights the genomic diversity of ETEC.
159 SR) analysis was further applied to identify ETEC-specific genomic regions when compared to non-ETEC
160 against the passenger domain of EatA impair ETEC delivery of labile toxin to epithelial cells sugges
164 s) have been identified and characterized in ETEC at least 30% of clinical ETEC isolates lack known C
165 ch also secretes LT, are highly conserved in ETEC and exist in other enteric pathogens, including oth
170 an autotransporter previously identified in ETEC, possesses a functional serine protease motif withi
172 ave examined specific regulatory networks in ETEC, although little is known about the global effects
178 tedly broad protective effects against LT(+) ETEC and mixed infections when using a toxin-based enter
180 1 allele variants were correlated with major ETEC lineages expressing CS1 + CS3 or CS2 + CS3, and the
182 Although this protein is expressed by many ETEC strains and is highly immunogenic, its precise func
183 ericidal, upregulates the expression of many ETEC virulence factors, including heat-stable (estA) and
184 urface antigen 20 (CS20) fimbriae as a model ETEC colonization factor, we show using force spectrosco
188 escent human sera obtained following natural ETEC infections demonstrated multiple immunoreactive mol
190 conserved among ETEC genomes than among non-ETEC E. coli genomes, suggesting that ETEC isolates shar
191 pecific genomic regions when compared to non-ETEC genomes, as well as genes that are more associated
192 ese studies suggest that CexE may be a novel ETEC virulence factor because its expression is controll
194 Particularly, passive oral administration of ETEC anti-fimbrial antibodies prevent ETEC diarrhea.
196 an important role for ECP in the biology of ETEC, particularly in CF-negative strains, and in human
197 sequencing of a representative collection of ETEC isolated between 1980 and 2011 identified globally
198 e that influences intestinal colonization of ETEC by degrading the major mucins in the small intestin
200 he conventional methods for the detection of ETEC, Vibrio, Y. enterocolitica, and P. shigelloides in
213 his hypothesis, we used an in vitro model of ETEC adherence to examine the role of LT in promoting ba
214 ere use a recently developed murine model of ETEC intestinal colonization to examine the immunogenici
215 , we found that a major effector molecule of ETEC, the heat-labile enterotoxin (LT), may enhance thes
216 in gene expression and surface morphology of ETEC upon interaction with intestinal epithelial cells i
218 itional insight into the intricate nature of ETEC interactions with the intestinal epithelium that ha
219 dies establish the relative pathogenicity of ETEC expressing newer class 5 fimbriae and suggest suita
222 es of a geographically diverse population of ETEC elaborating CFA/I (n = 31), CS17 (n = 20), and CS2
224 , an immunogenic secreted serine protease of ETEC, contributes to virulence by degrading MUC2, the ma
225 points were to investigate the field rate of ETEC diarrhoea, and to assess the safety of heat-labile
230 These studies increase our understanding of ETEC evolution, as well as provide insight into virulenc
234 hylogenetic distribution of clinical porcine ETEC strains and their plasmid-associated genetic conten
236 presented that probe the ability of porcine ETEC isolates to induce apoptosis and cell death in porc
237 ea revealed that a limited subset of porcine ETEC lineages exist that generally contain common toxin
240 ces of K88-positive and F18-positive porcine ETEC strains and examined the phylogenetic distribution
246 enterotoxins and pathogenicity during repeat ETEC infections appears to be variable and dependent on
249 Here we demonstrate that YghJ, a secreted ETEC antigen identified in immunoproteomic studies using
250 unction blocked the activity of the secreted ETEC factor, suggesting that this yet-uncharacterized ac
251 lonization factor genes across all sequenced ETEC genomes not only identified variability but also in
252 alignment method demonstrated that sequenced ETEC strains share approximately 2.7 million bases of ge
253 in the placebo group had moderate or severe ETEC diarrhoea (vaccine efficacy 34.6%, -2.2 to 58.9; p=
257 ting five pathogens (rotavirus, Shigella, ST-ETEC, Cryptosporidium, typical enteropathogenic E coli)
258 erichia coli producing heat-stable toxin (ST-ETEC; with or without co-expression of heat-labile enter
259 ed with increased risk of case death were ST-ETEC (hazard ratio [HR] 1.9; 0.99-3.5) and typical enter
260 ains were more closely related to human ST23 ETEC than to APEC O1, indicating that separation of path
266 sure following ETEC infection suggested that ETEC induced changes in plasma membrane asymmetry, indep
270 lusion, naturally occurring mutations in the ETEC adhesive and non-adhesive subunits altered function
272 genome" confirmed the diverse history of the ETEC pathovar and provides a finer resolution of the E.
274 noprecipitation experiments suggest that the ETEC factor functions by preventing IkappaBalpha polyubi
275 ponses corroborating reduced exposure to the ETEC pathogen, and a significantly higher weight gain co
281 We report that mice repeatedly exposed to ETEC are protected from subsequent colonization and that
285 protects against LT and LT/heat-stable toxin ETEC disease in the field, was 6,741 EU (a 3.3-fold incr
287 enged 30 healthy adults with an unattenuated ETEC strain, and collected serial blood samples shortly
288 ic analyses of 94 previously uncharacterized ETEC isolates demonstrated remarkable genomic diversity,
289 ave important implications for understanding ETEC pathogenesis, unraveling immunologic responses indu
290 n, 31 volunteers received product, underwent ETEC challenge, and were included in the per protocol ef
291 dings from the first challenge studies using ETEC-expressing colonization factor fimbria CS17 and CS1
296 Pretreating intestinal epithelial cells with ETEC supernatant significantly blocked the degradation o
298 relevant chemical signals were combined with ETEC isolate E24377A during growth in either Luria broth
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