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1 e against an epithelium-associated pathogen (Citrobacter rodentium).
2 e differentiating in response to a pathogen (Citrobacter rodentium).
3 CD4(+)CD45RB(hi) T cells, or infection with Citrobacter rodentium.
4 specially in the colon during infection with Citrobacter rodentium.
5 Salmonella enterica serovar Typhimurium and Citrobacter rodentium.
6 improves host tolerance of the mild pathogen Citrobacter rodentium.
7 evere colitis and death after infection with Citrobacter rodentium.
8 PEC and EHEC) and the natural mouse pathogen Citrobacter rodentium.
9 istration of dextran sulfate sodium (DSS) or Citrobacter rodentium.
10 ppled responses to intestinal infection with Citrobacter rodentium.
11 nce of the attaching/effacing mouse pathogen Citrobacter rodentium.
12 ir selective depletion during infection with Citrobacter rodentium.
13 itical for the clearance of the A/E pathogen Citrobacter rodentium.
14 ty against an intestinal bacterial pathogen, Citrobacter rodentium.
15 unity to the attaching-and-effacing pathogen Citrobacter rodentium.
16 zene sulfonic-acid (TNBS); or infection with Citrobacter rodentium.
17 ease induced by the model bacterial pathogen Citrobacter rodentium.
18 h the enteric pathogens Escherichia coli and Citrobacter rodentium.
19 uced colonization levels of the gut pathogen Citrobacter rodentium.
20 and ILFs in the colon during infection with Citrobacter rodentium.
21 nged orally with the enteric murine pathogen Citrobacter rodentium.
22 hanced resistance to the intestinal pathogen Citrobacter rodentium.
23 onization of the mouse colon by the bacteria Citrobacter rodentium.
24 the gram-negative enteric bacterial pathogen Citrobacter rodentium.
25 on with the gram-negative bacterial pathogen Citrobacter rodentium.
26 ost protection against a bacterial pathogen, Citrobacter rodentium.
27 ted in the A/E-lesion-forming mouse pathogen Citrobacter rodentium.
28 enteropathogenic Escherichia coli (EPEC) and Citrobacter rodentium.
29 a of mice infected with the enteric pathogen Citrobacter rodentium.
30 riage of the lethal enteric murine pathogen, Citrobacter rodentium.
31 almonella typhimurium, Shigella flexneri and Citrobacter rodentium.
32 local and systemic bacterial infection with Citrobacter rodentium.
33 s the effectiveness of oral vaccines against Citrobacter rodentium.
34 scherichia coli and their murine equivalent, Citrobacter rodentium.
35 nths in an activated state after exposure to Citrobacter rodentium.
36 cute colitis induced by the enteric pathogen Citrobacter rodentium.
37 rial infection with the noninvasive pathogen Citrobacter rodentium.
38 ction against early-life lethal infection by Citrobacter rodentium.
39 long with the anti-swarming activity against Citrobacter rodentium.
40 tion of mice by the EPEC-like mouse pathogen Citrobacter rodentium.
41 more aggressive infectious colitis caused by Citrobacter rodentium.
42 and lethal colitis by the mucosal pathogen, Citrobacter rodentium.
43 infection with the EPEC-like mouse pathogen Citrobacter rodentium.
44 impaired gut colonization resistance against Citrobacter rodentium.
45 rves in the coordination of host defenses to Citrobacter rodentium.
46 onse to the attaching and effacing bacterium Citrobacter rodentium.
47 mpaired clearance of the intestinal pathogen Citrobacter rodentium.
48 of Runx3 in ILCs exacerbated infection with Citrobacter rodentium.
49 with LPS or infected with the enteropathogen Citrobacter rodentium.
50 ssential for the protective immunity against Citrobacter rodentium.
53 at germ-free animals are unable to eradicate Citrobacter rodentium, a model for human infections with
54 reover, mice lacking TACI were able to clear Citrobacter rodentium, a model pathogen for severe human
55 acid L-tryptophan protects the host against Citrobacter rodentium, a mouse AE pathogen that is widel
56 C, we constructed an Stx-producing strain of Citrobacter rodentium, a murine AE pathogen that otherwi
57 s derived from these mice were infected with Citrobacter rodentium, a murine attaching and effacing p
67 cute colitis induced by the enteric pathogen Citrobacter rodentium Adoptive transfer of macrophage-ri
69 the murine gut microbiome to infection with Citrobacter rodentium, an attaching-and-effacing bacteri
70 e exhibited impaired intestinal clearance of Citrobacter rodentium, an enteric bacterium that models
72 wnregulation of virulence gene expression in Citrobacter rodentium, an enteric pathogen that models h
74 ching and effacing (AE) pathogens, including Citrobacter rodentium and enteropathogenic Escherichia c
76 ly within the colon of BT-11-treated mice in Citrobacter rodentium and IL-10(-/-) mouse models of col
77 acterium bovis bacillus Calmette-Guerin, and Citrobacter rodentium and of tumor growth in a syngeneic
79 context of infection with the enteropathogen Citrobacter rodentium and that its presence is central f
80 y divergent enteric pathogens, the bacterium Citrobacter rodentium and the helminth Heligmosomoides p
81 P3 activators LPS and ATP, Escherichia coli, Citrobacter rodentium and transfection of LPS, AIM2 acti
82 ike toxin-producing E. coli, E. coli RDEC-1, Citrobacter rodentium, and an EPEC espB insertion mutant
83 hesins of enteropathogenic Escherichia coli, Citrobacter rodentium, and enterohemorrhagic E. coli (EH
84 tary intervention, mice were challenged with Citrobacter rodentium, and pathological responses were a
86 usceptible strain of the pathogenic bacteria Citrobacter rodentium, and we propose a general approach
87 erichia coli, enterohemorrhagic E. coli, and Citrobacter rodentium are classified as attaching and ef
88 erichia coli, enterohemorrhagic E. coli, and Citrobacter rodentium are classified as attaching and ef
89 e surrogate murine infection model for EHEC, Citrobacter rodentium, are all examples of microorganism
90 ice, we employed the natural murine pathogen Citrobacter rodentium as a model of EHEC virulence to in
94 The attaching and effacing mouse pathogen Citrobacter rodentium associates intimately with the int
95 lonization by the enteric bacterial pathogen Citrobacter rodentium by consuming amino acids, thus sta
96 for IEC-intrinsic IL-1R are unable to clear Citrobacter rodentium (C. rodentium) but are protected f
97 nificantly increased bacterial burden during Citrobacter rodentium (C. rodentium) infection in mice.
99 d cell (ILC) and T cell-derived IL-22 during Citrobacter rodentium (C.r) infection using mice that bo
100 artonella spp., Lawsonia intracellularis and Citrobacter rodentium) can induce cellular proliferation
101 ore severe pneumonia, whereas infection with Citrobacter rodentium caused worse inflammatory colitis
105 We demonstrate that after infection with Citrobacter rodentium, CD4(+) LTi cells were a dominant
108 e more susceptible to enteric infection with Citrobacter rodentium compared to wild-type (WT) mice ev
109 es after exposure to the intestinal pathogen Citrobacter rodentium Correspondingly, AQP3(-/-) mice sh
110 crypts at days 6 and 12 post-infection with Citrobacter rodentium (CR) and tended to decline at days
111 (EPEC), enterohemorrhagic E. coli (EHEC) and Citrobacter rodentium (CR) infections, are dependent on
113 sent a genetics-based platform that utilises Citrobacter rodentium (CR), an enteric mouse pathogen, t
114 idly succumb when exposed to murine pathogen Citrobacter rodentium (CR), whereas pups fostered on com
117 population of the diarrhea causing bacterium Citrobacter rodentium during colonization of its natural
121 Lymphocyte inhibitory factor A (lifA) in Citrobacter rodentium encodes the large toxin lymphostat
123 infected with Gram-negative bacteria such as Citrobacter rodentium, Escherichia coli, or Pseudomonas
125 a coli (EPEC)-mediated disease in humans and Citrobacter rodentium (formerly C. freundii biotype 4280
127 ontrolled spread of the pathogenic bacterium Citrobacter rodentium from infected to naive female anim
128 also required for clearance of the bacterium Citrobacter rodentium from the gastrointestinal tract.
130 tion of pathogenic Th17 cells in response to Citrobacter rodentium; however, there is no effect on no
134 lock the pathogenesis of the murine pathogen Citrobacter rodentium In this work, we aimed to gain a b
135 ry response to the colitis-inducing pathogen Citrobacter rodentium in vitro by inhibiting NF-kappaB a
137 activated by the colitis-inducing bacterium Citrobacter rodentium increased NO without affecting iNO
138 romote early protection against the pathogen Citrobacter rodentium, independent of CD4(+) T cells.
139 ride (LPS) and infection with mouse pathogen Citrobacter rodentium induce translocation of the nuclea
141 entrations of fecal acylcarnitines in murine Citrobacter rodentium-induced colitis and human inflamma
145 ucosa-associated microbiota, and exacerbates Citrobacter rodentium-induced inflammation, effects that
150 bile from specific-pathogen-free, germ-free, Citrobacter rodentium-infected or Listeria monocytogenes
151 airway inflammation and influenza A virus or Citrobacter rodentium infection along with metagenomics
152 milarly opposing phenotypes were observed in Citrobacter rodentium infection and allergic asthma.
153 22 receptor IL-22RA1 protects against lethal Citrobacter rodentium infection and chemical-induced col
154 anced and associated with protection against Citrobacter rodentium infection and exacerbation of dext
155 C3 proliferation and host protection against Citrobacter rodentium infection and metabolically affect
156 sease, whereas expansion of these cells upon Citrobacter rodentium infection exacerbated pathology.
157 lsion, caused by a deficit in ILC2s, whereas Citrobacter rodentium infection is cleared efficiently.
159 ization following microbiome disruption with Citrobacter rodentium infection or antibiotic treatment,
160 disease impact, SDR was combined with either Citrobacter rodentium infection or dextran sulfate sodiu
161 nt mice are less able to eradicate a mucosal Citrobacter rodentium infection than wild-type C57BL/6 m
163 ency increased morbidity and mortality after Citrobacter rodentium infection with decreased secretion
165 provides that link for the investigation of Citrobacter rodentium infection, a mouse model for enter
166 t mice exhibited increased susceptibility to Citrobacter rodentium infection, associated with the inc
167 testinal epithelial cells after T. gondii or Citrobacter rodentium infection, but also maintained the
168 KKbeta(DeltaIEC) mice efficiently controlled Citrobacter rodentium infection, IKKalpha(DeltaIEC) mice
173 impaired mouse antibacterial defense against Citrobacter rodentium infection, which was associated wi
174 nate inflammatory RelA/NF-kappaB response to Citrobacter rodentium infection, while Nfkb2(-/-) mice s
191 ons that T-helper cell, type 17 responses in Citrobacter rodentium infections are driven by concomita
207 that enterohaemorrhagic Escherichia coli and Citrobacter rodentium, its surrogate in a mouse infectio
208 bacterial family member and murine pathogen Citrobacter rodentium, its virulence strategy likely inv
210 after infection with the intestinal pathogen Citrobacter rodentium, leading to impaired survival.
211 resistance against a murine enteropathogen, Citrobacter rodentium, leading to the death of the anima
215 hage activation and disease phenotype in the Citrobacter rodentium model of murine infectious colitis
216 that in both the dextran sodium sulfate and Citrobacter rodentium models of colitis, significantly i
217 (EHEC), enteropathogenic E. coli (EPEC), and Citrobacter rodentium Moreover, Salmonella enterica stra
220 ing infection by the murine enteric pathogen Citrobacter rodentium of the family Enterobacteriacea.
222 ute colitis was induced by administration of Citrobacter rodentium or dextran sulfate sodium (DSS) to
225 with EPEC, using the mouse-specific pathogen Citrobacter rodentium Our murine infant model is similar
226 n of adult females with the enteric pathogen Citrobacter rodentium protects dams and offspring agains
227 , and the introduction of the enteropathogen Citrobacter rodentium reproducibly promotes rapid select
229 in the context of intestinal infection with Citrobacter rodentium, resulting in preserved innate imm
230 mice with the intestinal bacterial pathogen Citrobacter rodentium results in colonic mucosal hyperpl
232 egative bacteria including Escherichia coli, Citrobacter rodentium, Salmonella typhimurium, and Shige
233 nterohemorrhagic Escherichia coli (EHEC) and Citrobacter rodentium sense and utilize galacturonic aci
236 uction in the intestines upon infection with Citrobacter rodentium, the percentage of IgA(+)CD38(+)CD
237 m highly susceptible to the enteric pathogen Citrobacter rodentium This heightened susceptibility to
238 ies have found the murine bacterial pathogen Citrobacter rodentium to provide a robust, relevant in-v
242 EPEC), as well as the related mouse pathogen Citrobacter rodentium, utilize a type III secretion syst
245 rine infection model with one such pathogen, Citrobacter rodentium, was used to elucidate the importa
246 ice with the attaching and effacing bacteria Citrobacter rodentium, we defined the mechanisms and con
247 ty transposon screen in the enteric pathogen Citrobacter rodentium, we find that the bacterium requir
250 diated inflammation and host defense against Citrobacter rodentium were not impaired in the absence o
251 d inflammation by the enteric mouse pathogen Citrobacter rodentium, which causes disease similar to t
252 d the murine attaching and effacing pathogen Citrobacter rodentium, which colonizes primarily the sur
253 nse generated to the extracellular bacterium Citrobacter rodentium, which induces a mixed Th1 and Th1
254 ArgR also augments murine disease caused by Citrobacter rodentium, which is a murine pathogen extens
255 activity against the murine enteric pathogen Citrobacter rodentium, which like the related clinically
256 testinal epithelium with the rodent pathogen Citrobacter rodentium, which models human infections wit
257 ptible than wild-type mice to infection with Citrobacter rodentium, which suggests a role for PMR in
258 dered indispensable for host defence against Citrobacter rodentium, with 100% mortality of Il22(-/-)