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1 almonella clade (which includes Shigella and Citrobacter).
3 rs of the genera Vibrio , Enterobacter , and Citrobacter and by Bacillus stratosphericus was confirme
6 ignificantly inhibited autophagic killing of Citrobacter, attesting to the functional importance of t
7 (CYP176A1) is a bacterial P450 isolated from Citrobacter braakii that catalyzes the hydroxylation of
10 nts and established that mouse mortality and Citrobacter colonization were reduced in mice infected w
11 more resistant to intestinal colonization by Citrobacter, developed lower levels of serum Citrobacter
12 ther strains of Salmonella as well as within Citrobacter, Erwinia, Escherichia, Photorhabdus, and Yer
14 sinia intermedia, Kluyvera cryocrescens, and Citrobacter farmeri but identification scores were low a
15 studies on infant rats have documented many Citrobacter-filled macrophages within the ventricles and
18 ll-free supernatants from Proteus mirabilis, Citrobacter freundii and Enterobacter agglomerans [cyclo
19 detected in carbapenem-resistant isolates of Citrobacter freundii and Klebsiella oxytoca recovered fr
27 e (WT) forms, such as the E. cloacae P99 and Citrobacter freundii enzymes, the ES GC1 beta-lactamase
28 iae, Klebsiella oxytoca, Citrobacter koseri, Citrobacter freundii group, Enterobacter spp., and Serra
34 lle and propanediol utilization enzymes from Citrobacter freundii is fully functional when cloned in
35 lococcus aureus, Pseudomonas aeruginosa, and Citrobacter freundii to ensure the species specificity o
36 ophan indole-lyase and to wild type and Y71F Citrobacter freundii tyrosine phenol-lyase was investiga
37 he molecular interactions between AmpR (from Citrobacter freundii), its DNA operator, and repressor U
38 tatively for Gram-negative Escherichia coli, Citrobacter freundii, and Enterobacter aerogenes, as wel
39 with colonization of the intestinal tract by Citrobacter freundii, Clostridium species, Enterobacter
40 c inhibition was also observed in strains of Citrobacter freundii, Klebsiella pneumoniae, Enterobacte
41 ve selectivity of these ligands for E. coli, Citrobacter freundii, Staphylococcus epidermidis were 10
42 lococcus aureus, Pseudomonas aeruginosa, and Citrobacter freundii, to ensure the species-specificity
43 five enterobacteria (Salmonella typhimurium, Citrobacter freundii, Yersinia enterocolitica, Serratia
49 strains of Citrobacter genomospecies 10 and Citrobacter genomospecies 11 were identified, allowing t
50 rmerly Citrobacter freundii biotype 4280 and Citrobacter genomospecies 9) was described on the basis
51 lowing these species to be formally named as Citrobacter gillenii sp. nov. and Citrobacter murliniae
54 To directly test whether RELMalpha promoted Citrobacter-induced intestinal inflammation via IL-17A,
57 s previously inaccessible information on how Citrobacter infection and clearance reshapes the gut mic
58 e stimulatory effects of RELMalpha following Citrobacter infection were pathologic rather than host-p
60 ia coli strain UTI89 and by enteric bacteria Citrobacter koseri and Salmonella enterica serovar typhi
61 S rDNA sequence was 97.8% similar to that of Citrobacter koseri but 97.0% similar to that of Enteroba
66 richia coli, Salmonella typhimurium LT2, and Citrobacter koseri were able to cross-seed in vitro.
67 , Klebsiella pneumoniae, Klebsiella oxytoca, Citrobacter koseri, Citrobacter freundii group, Enteroba
68 terization of a novel bacterial homolog from Citrobacter koseri, CLC-ck2, has yielded surprising disc
71 nine species, including the first isolate of Citrobacter koserii and Morganella morganii known to har
72 the coinfected mice was correlated with high Citrobacter loads in the gut, translocation of the bacte
76 logous genes in Escherichia, Salmonella, and Citrobacter, or E. coli, E. fergusonii, and E. albertii.
79 (EPEC), enterohemorrhagic E. coli (EHEC) and Citrobacter rodentium (CR) infections, are dependent on
84 a coli (EPEC)-mediated disease in humans and Citrobacter rodentium (formerly C. freundii biotype 4280
86 cute colitis induced by the enteric pathogen Citrobacter rodentium Adoptive transfer of macrophage-ri
90 P3 activators LPS and ATP, Escherichia coli, Citrobacter rodentium and transfection of LPS, AIM2 acti
91 erichia coli, enterohemorrhagic E. coli, and Citrobacter rodentium are classified as attaching and ef
92 erichia coli, enterohemorrhagic E. coli, and Citrobacter rodentium are classified as attaching and ef
95 The attaching and effacing mouse pathogen Citrobacter rodentium associates intimately with the int
101 es after exposure to the intestinal pathogen Citrobacter rodentium Correspondingly, AQP3(-/-) mice sh
103 Lymphocyte inhibitory factor A (lifA) in Citrobacter rodentium encodes the large toxin lymphostat
104 also required for clearance of the bacterium Citrobacter rodentium from the gastrointestinal tract.
108 ry response to the colitis-inducing pathogen Citrobacter rodentium in vitro by inhibiting NF-kappaB a
110 activated by the colitis-inducing bacterium Citrobacter rodentium increased NO without affecting iNO
111 ride (LPS) and infection with mouse pathogen Citrobacter rodentium induce translocation of the nuclea
115 milarly opposing phenotypes were observed in Citrobacter rodentium infection and allergic asthma.
116 22 receptor IL-22RA1 protects against lethal Citrobacter rodentium infection and chemical-induced col
117 sease, whereas expansion of these cells upon Citrobacter rodentium infection exacerbated pathology.
118 lsion, caused by a deficit in ILC2s, whereas Citrobacter rodentium infection is cleared efficiently.
120 ization following microbiome disruption with Citrobacter rodentium infection or antibiotic treatment,
121 nt mice are less able to eradicate a mucosal Citrobacter rodentium infection than wild-type C57BL/6 m
123 ency increased morbidity and mortality after Citrobacter rodentium infection with decreased secretion
125 provides that link for the investigation of Citrobacter rodentium infection, a mouse model for enter
126 testinal epithelial cells after T. gondii or Citrobacter rodentium infection, but also maintained the
127 KKbeta(DeltaIEC) mice efficiently controlled Citrobacter rodentium infection, IKKalpha(DeltaIEC) mice
130 nate inflammatory RelA/NF-kappaB response to Citrobacter rodentium infection, while Nfkb2(-/-) mice s
140 ons that T-helper cell, type 17 responses in Citrobacter rodentium infections are driven by concomita
156 hage activation and disease phenotype in the Citrobacter rodentium model of murine infectious colitis
157 that in both the dextran sodium sulfate and Citrobacter rodentium models of colitis, significantly i
158 (EHEC), enteropathogenic E. coli (EPEC), and Citrobacter rodentium Moreover, Salmonella enterica stra
160 ing infection by the murine enteric pathogen Citrobacter rodentium of the family Enterobacteriacea.
161 ute colitis was induced by administration of Citrobacter rodentium or dextran sulfate sodium (DSS) to
163 with EPEC, using the mouse-specific pathogen Citrobacter rodentium Our murine infant model is similar
165 mice with the intestinal bacterial pathogen Citrobacter rodentium results in colonic mucosal hyperpl
168 ies have found the murine bacterial pathogen Citrobacter rodentium to provide a robust, relevant in-v
173 artonella spp., Lawsonia intracellularis and Citrobacter rodentium) can induce cellular proliferation
176 at germ-free animals are unable to eradicate Citrobacter rodentium, a model for human infections with
177 reover, mice lacking TACI were able to clear Citrobacter rodentium, a model pathogen for severe human
178 C, we constructed an Stx-producing strain of Citrobacter rodentium, a murine AE pathogen that otherwi
179 s derived from these mice were infected with Citrobacter rodentium, a murine attaching and effacing p
187 the murine gut microbiome to infection with Citrobacter rodentium, an attaching-and-effacing bacteri
188 e exhibited impaired intestinal clearance of Citrobacter rodentium, an enteric bacterium that models
190 wnregulation of virulence gene expression in Citrobacter rodentium, an enteric pathogen that models h
191 ike toxin-producing E. coli, E. coli RDEC-1, Citrobacter rodentium, and an EPEC espB insertion mutant
192 hesins of enteropathogenic Escherichia coli, Citrobacter rodentium, and enterohemorrhagic E. coli (EH
193 tary intervention, mice were challenged with Citrobacter rodentium, and pathological responses were a
194 usceptible strain of the pathogenic bacteria Citrobacter rodentium, and we propose a general approach
195 e surrogate murine infection model for EHEC, Citrobacter rodentium, are all examples of microorganism
197 We demonstrate that after infection with Citrobacter rodentium, CD4(+) LTi cells were a dominant
198 after infection with the intestinal pathogen Citrobacter rodentium, leading to impaired survival.
199 resistance against a murine enteropathogen, Citrobacter rodentium, leading to the death of the anima
200 in the context of intestinal infection with Citrobacter rodentium, resulting in preserved innate imm
202 egative bacteria including Escherichia coli, Citrobacter rodentium, Salmonella typhimurium, and Shige
203 EPEC), as well as the related mouse pathogen Citrobacter rodentium, utilize a type III secretion syst
204 rine infection model with one such pathogen, Citrobacter rodentium, was used to elucidate the importa
205 ice with the attaching and effacing bacteria Citrobacter rodentium, we defined the mechanisms and con
207 d inflammation by the enteric mouse pathogen Citrobacter rodentium, which causes disease similar to t
208 d the murine attaching and effacing pathogen Citrobacter rodentium, which colonizes primarily the sur
209 nse generated to the extracellular bacterium Citrobacter rodentium, which induces a mixed Th1 and Th1
210 activity against the murine enteric pathogen Citrobacter rodentium, which like the related clinically
211 testinal epithelium with the rodent pathogen Citrobacter rodentium, which models human infections wit
214 ucosa-associated microbiota, and exacerbates Citrobacter rodentium-induced inflammation, effects that
257 omass could be reutilized as a substrate for Citrobacter sp. AzoR-1 cultivation and bioflocculant pro
260 d DNA-DNA hybridization data and is the only Citrobacter species known to possess virulence factors h
261 In addition, opportunistic infections with Citrobacter species or Klebsiella species occurred only
263 istance against Clostridium, Salmonella, and Citrobacter species, researchers are now exploring mecha
266 Citrobacter, developed lower levels of serum Citrobacter-specific IgM and IgG antibodies following or
268 s growing Enterobacter spp, Serratia spp, or Citrobacter spp were evaluated using the cefotetan-boron
269 cter spp. (13), Enterobacter aerogenes (11), Citrobacter spp. (10), Pseudomonas spp. (non P. aerugino
270 the chromosomal enzymes of Enterobacter and Citrobacter spp. and also mediate resistance to extended
273 an effort to understand the pathogenesis of Citrobacter spp. causing meningitis, we have used the in
275 , P. aeruginosa, and S. marcescens, 5/6 with Citrobacter spp., 13/14 with Enterobacter spp., 23/24 wi
276 solates of Enterobacter spp., Serratia spp., Citrobacter spp., and Pseudomonas aeruginosa were evalua
277 9 genus/species targets (Acinetobacter spp., Citrobacter spp., Enterobacter spp., Escherichia coli/Sh
278 lmonella spp., Shigella spp., Yersinia spp., Citrobacter spp., enterotoxigenic (ETEC) and enteroaggre
281 Complementing DeltanleH with NleH1 restored Citrobacter virulence and colonization to wild-type leve
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