ライフサイエンスコーパス: rodentium

1 e anti-swarming activity against Citrobacter rodentium.

2 by the EPEC-like mouse pathogen Citrobacter rodentium.

3 rance of the intestinal pathogen Citrobacter rodentium.

4 ILCs exacerbated infection with Citrobacter rodentium.

5 infected with the enteropathogen Citrobacter rodentium.

6 the protective immunity against Citrobacter rodentium.

7 ned the sensitivity of Cxcr6(-/-) mice to C. rodentium.

8 the colon during infection with Citrobacter rodentium.

9 enterica serovar Typhimurium and Citrobacter rodentium.

10 class 1 SPATE null mutant (Deltacrc1) in C. rodentium.

11 n D-deficient diet and then infected with C. rodentium.

12 t tolerance of the mild pathogen Citrobacter rodentium.

13 cells during host defense in mice against C. rodentium.

14 s and death after infection with Citrobacter rodentium.

15 ) and the natural mouse pathogen Citrobacter rodentium.

16 dextran sulfate sodium (DSS) or Citrobacter rodentium.

17 was sufficient for direct binding to EPEC/C. rodentium.

18 endritic cells, were impaired in clearing C. rodentium.

19 r a resistant mouse highly susceptible to C. rodentium.

20 esion forming bacterial pathogens such as C. rodentium.

21 ses to intestinal infection with Citrobacter rodentium.

22 ttaching/effacing mouse pathogen Citrobacter rodentium.

23 depletion during infection with Citrobacter rodentium.

24 he clearance of the A/E pathogen Citrobacter rodentium.

25 n intestinal bacterial pathogen, Citrobacter rodentium.

26 attaching-and-effacing pathogen Citrobacter rodentium.

27 after administration of ethanol, TNBS, or C rodentium.

28 c-acid (TNBS); or infection with Citrobacter rodentium.

29 ive infectious colitis caused by Citrobacter rodentium.

30 uring challenge with the colonic pathogen C. rodentium.

31 by the model bacterial pathogen Citrobacter rodentium.

32 ense against enteric infections caused by C. rodentium.

33 c pathogens Escherichia coli and Citrobacter rodentium.

34 e infected by oral gavage with pathogenic C. rodentium.

35 ation levels of the gut pathogen Citrobacter rodentium.

36 the colon during infection with Citrobacter rodentium.

37 atenin signaling and host defense against C. rodentium.

38 with the enteric murine pathogen Citrobacter rodentium.

39 epithelial barrier compromise induced by C. rodentium.

40 ide enhanced protection to infection with C. rodentium.

41 colitis by the mucosal pathogen, Citrobacter rodentium.

42 ith the EPEC-like mouse pathogen Citrobacter rodentium.

43 by ILC3s and impaired innate immunity to C. rodentium.

44 colonization resistance against Citrobacter rodentium.

45 it was required for host defense against C. rodentium.

46 attaching and effacing bacterium Citrobacter rodentium.

47 In mice infected with Citrobacter rodentium, a model for enteropathogenic Escherichia coli

48 animals are unable to eradicate Citrobacter rodentium, a model for human infections with attaching a

49 lacking TACI were able to clear Citrobacter rodentium, a model pathogen for severe human enteritis,

50 ucted an Stx-producing strain of Citrobacter rodentium, a murine AE pathogen that otherwise lacks Stx

51 om these mice were infected with Citrobacter rodentium, a murine attaching and effacing pathogen rela

52 Citrobacter rodentium, a murine model pathogen that shares important

53 /6 mice were orally gavaged with Citrobacter rodentium, a murine pathogen related to human diarrheage

54 otics prevent disease induced by Citrobacter rodentium, a murine-specific enteric pathogen.

55 Infection with Citrobacter rodentium, a natural mouse pathogen homologous to EHEC,

56 Citrobacter rodentium, a natural mouse pathogen, has recently been s

57 nst the pathogen, phenotypically virulent C. rodentium, accumulated and infected the epithelium and s

58 C. rodentium activated DC especially in colon-draining LNs,

59 induced by the enteric pathogen Citrobacter rodentium Adoptive transfer of macrophage-rich peritonea

60 the extracellular enteropathogen Citrobacter rodentium after phagocytosis.

61 traint stressor prior to a challenge with C. rodentium alters the intestinal microbiota community str

62 gut microbiome to infection with Citrobacter rodentium, an attaching-and-effacing bacterium that prov

63 impaired intestinal clearance of Citrobacter rodentium, an enteric bacterium that models human infect

64 of virulence gene expression in Citrobacter rodentium, an enteric pathogen that models human infecti

65 esistance and in the pathology induced by C. rodentium, an infection that mimics disease caused by co

66 t acute bacterial infection with Citrobacter rodentium and Clostridium difficile.

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

68 Citrobacter rodentium and Escherichia coli O157 triggered similar Th

69 ed key information about the phylogeny of C. rodentium and identified 1,585 C. rodentium-specific (wi

70 iency of Cyba resulted in protection from C. rodentium and L. monocytogenes infection.

71 s LPS and ATP, Escherichia coli, Citrobacter rodentium and transfection of LPS, AIM2 activators Franc

72 C57BL/6 mice were infected with C. rodentium and treated with dimethyl sulfoxide (DMSO) (ve

73 lt and neonatal mice were challenged with C. rodentium, and a probiotic mixture containing Lactobacil

74 ry response after administration of DSS or C rodentium, and intestine-specific overexpression of EPAS

75 ntion, mice were challenged with Citrobacter rodentium, and pathological responses were assessed.

76 colonic microbiota during challenge with C. rodentium, and that these effects are long-lasting and n

77 train of the pathogenic bacteria Citrobacter rodentium, and we propose a general approach for exploit

78 e mucus layer, leading to amelioration of C. rodentium- and DBZ-induced colitis in NIH:Swiss mice.

79 Production of C. rodentium antigen-specific IgM and IgG antibodies was no

80 Among the 29 T3SS effectors found in C. rodentium are all 22 of the core effectors of EPEC strai

81 murine infection model for EHEC, Citrobacter rodentium, are all examples of microorganisms that modul

82 In this study, we employed Citrobacter rodentium as a physiologic model of pathogenic Escherich

83 hCD98 Tg mice) and infected with Citrobacter rodentium as an in vivo model.

84 Using C. rodentium as an infection model, and dextran sulfate sod

85 attaching and effacing pathogen, Citrobacter rodentium, as a potential drug target.

86 e that IL-10 is dispensable for resolving C. rodentium-associated colitis and further suggest that IL

87 found in the gut of mammals, could reduce C. rodentium-associated disease, mice received wild-type B.

88 , respectively, did not protect mice from C. rodentium-associated disease.

89 zed EPS and showed that they also prevent C. rodentium-associated intestinal disease after a single i

90 hing and effacing mouse pathogen Citrobacter rodentium associates intimately with the intestinal epit

91 ce lacking DOCK2 were more susceptible to C. rodentium attachment to intestinal epithelial cells.

92 These mice harbored increased levels of C. rodentium bacteria, showed more pronounced weight loss a

93 GC-C-/- mice had an increase in C. rodentium bacterial load in stool relative to GC-C+/+.

94 was associated with an altered pattern of C. rodentium bacterial migration.

95 tic diarrhea reduced colitis severity and C. rodentium burden in claudin-2-deficient, but not transge

96 ged colonization associated with a higher C. rodentium burden in gastrointestinal tissue and spread i

97 equired for survival after infection with C. rodentium, but CD103(+) cDCs dependent on the transcript

98 t only contribute to host defense against C. rodentium, but provide protection against infection-asso

99 production of IL-22 during infection with C. rodentium, but the lymphotoxin-like protein LIGHT did no

100 cally ablated (GC-C-/-) were administered C. rodentium by orogastric gavage and analyzed at multiple

101 efore or 12 h after oral inoculation with C. rodentium, caused highly significant attenuation of inte

102 Citrobacter rodentium causes epithelial hyperplasia and colitis and

103 strate that after infection with Citrobacter rodentium, CD4(+) LTi cells were a dominant source of in

104 e exposure to the stressor, on Day 6 post-C. rodentium challenge, and persisted for up to 19 days aft

105 ration of fucosylated oligosaccharides to C. rodentium-challenged Il22ra1(-/-) mice attenuated infect

106 null mice had impaired immune responses to C rodentium, characterized by decreased levels of colonic

107 With C. rodentium, COG112 improved the clinical parameters of su

108 Dextran sodium sulfate (DSS) and Citrobacter rodentium colitis (CC) was induced in adult mice and col

109 were found throughout expanded crypts in C. rodentium colitis.

110 pstream of Y451 and downstream of Y471 in C. rodentium colonization and A/E lesion formation.

111 NleB O-GlcNAcylation activity attenuates C. rodentium colonization of mice.

112 stressor led to a significant increase in C. rodentium colonization over that in nonstressed control

113 n were protected from disease even though C. rodentium colonization was not inhibited.

114 osure to the intestinal pathogen Citrobacter rodentium Correspondingly, AQP3(-/-) mice showed impaire

115 rohemorrhagic E. coli (EHEC) and Citrobacter rodentium (CR) infections, are dependent on the effector

116 Citrobacter rodentium (CR) promotes crypt hyperplasia and tumorigene

117 Utilizing the Citrobacter rodentium (CR)-induced transmissible murine colonic hype

118 model, using the mouse pathogen Citrobacter rodentium (CR).

119 Vitamin D-deficient mice challenged with C. rodentium demonstrated increased colonic hyperplasia and

120 Mice infected with Stx-producing C. rodentium developed AE lesions on the intestinal epithel

121 enic Escherichia coli (EPEC) and Citrobacter rodentium during mammalian infections.

122 essential for protective immunity against C. rodentium during the first 6 days after infection.

123 In addition, we identified a novel C. rodentium effector, named EspS.

124 e the stressor-enhanced susceptibility to C. rodentium-enhanced infectious colitis.

125 parts, PepT1 transgenic mice infected with C rodentium exhibited decreased bacterial colonization, pr

126 the mucosal surface and drove an aerobic C. rodentium expansion in the colon.

127 ichia coli (EPEC and EHEC, respectively), C. rodentium exploits a type III secretion system (T3SS) to

128 C. rodentium exposure was shown to increase ILK expression

129 erocytes isolated from mice infected with C. rodentium expressing Tir_Y451A/Y471A expressed significa

130 Citrobacter rodentium (formally Citrobacter freundii biotype 4280) i

131 d for clearance of the bacterium Citrobacter rodentium from the gastrointestinal tract.

132 C. rodentium harbors two type VI secretion systems (T6SS) (

133 In mice, susceptibility to Citrobacter rodentium has been shown to be dependent on host genetic

134 s to a common pool of mobile DNA and that C. rodentium has lost gene functions associated with a prev

135 mmasome signaling in host defense against C. rodentium has not been characterized.

136 ukin-17A production during infection with C. rodentium However, upon CD4 T cell transfer into Rag(-/-

137 nsistent with weakened innate immunity to C. rodentium, IKKalpha(DeltaIEC) mice displayed impaired IL

138 ve days and all mice were challenged with C. rodentium immediately following the first exposure to th

139 cytic cells, produced CCL2 in response to C. rodentium in a Nod2-dependent manner.

140 pregulated on day 12 after infection with C. rodentium in mice fed the doubly deficient diet compared

141 s and host defense against infection with C. rodentium in mice lacking lymphotoxin signals, which sug

142 olonic cells, increased the attachment of C. rodentium in mouse colons and resulted in increased expr

143 tably, the defective host defense against C. rodentium in Stat3(CD4) mice could be fully restored by

144 t diet for 6 weeks had increased loads of C. rodentium in the colon and spleen, which were not observ

145 mmune system selectively targets virulent C. rodentium in the intestinal lumen to promote pathogen er

146 of mouse colonic infection with Citrobacter rodentium in the presence of T cells.

147 attaching and effacing pathogen Citrobacter rodentium in these.

148 to the colitis-inducing pathogen Citrobacter rodentium in vitro by inhibiting NF-kappaB activation.

149 NK cells were also cytotoxic to C. rodentium in vitro.

150 7 agonist R848 or infection with Citrobacter rodentium in vivo.

151 y the colitis-inducing bacterium Citrobacter rodentium increased NO without affecting iNOS levels.

152 ta-catenin signaling and the clearance of C. rodentium independent of adaptive immune responses.

153 vivo and in vivo experiments revealed that C rodentium induced colonic PepT1 expression and that, com

154 found that the enteric pathogen Citrobacter rodentium induced sequential waves of IL-22-producing IL

155 ILK influences the host response to C. rodentium -induced infection, independently of reduced c

156 oadministration of probiotics ameliorated C. rodentium-induced barrier dysfunction, epithelial hyperp

157 barrier function in vitro and on Citrobacter rodentium-induced colitis in mice.

158 n, a positive regulator of complement, in C. rodentium-induced colitis.

159 pendent colitis was confirmed in Citrobacter rodentium-induced disease.

160 Moreover, C. rodentium-induced expansion and activation of intestinal

161 4, and caspase-1 were hypersusceptible to C. rodentium-induced gastrointestinal inflammation.

162 rolonged restraint significantly enhanced C. rodentium-induced infectious colitis in resistant mice,

163 which may contribute to stressor-enhanced C. rodentium-induced infectious colitis.

164 rotease that is critical for E. coli- and C. rodentium-induced inflammasome activation, but dispensab

165 Previous studies have suggested that C. rodentium-induced inflammation is associated with an inc

166 ated microbiota, and exacerbates Citrobacter rodentium-induced inflammation, effects that can be atte

167 ould protect IKKalpha(DeltaIEC) mice from C. rodentium-induced morbidity.

168 o facilitate crypt regeneration following C. rodentium-induced pathogenesis.

169 Utilizing C. rodentium-induced TMCH in C3H/HeNHsd inbred mice, we obs

170 Utilizing the Citrobacter rodentium-induced transmissible murine colonic hyperplas

171 Citrobacter rodentium induces transmissible murine colonic hyperplas

172 Citrobacter rodentium induces transmissible murine colonic hyperplas

173 CAIV, affect intestinal ion transport in C. rodentium-infected FVB and C3H mice, resulting in profou

174 cantly increased in the colonic tissue of C. rodentium-infected hCD98 Tg mice compared to that of WT

175 nistration of 6% pectin or 4% curcumin in C. rodentium-infected mice also inhibited NF-kappaB activit

176 inhibit T cell activation in vitro and in C. rodentium-infected mice.

177 sing phenotypes were observed in Citrobacter rodentium infection and allergic asthma.

178 IL-22RA1 protects against lethal Citrobacter rodentium infection and chemical-induced colitis by prom

179 t IL-7 is produced by IECs in response to C. rodentium infection and plays a critical role in the pro

180 N-gamma activated the mucosal immunity to C. rodentium infection by increasing the expression of infl

181 However, NleB delivery during EPEC and C. rodentium infection caused rapid and preferential modifi

182 as expansion of these cells upon Citrobacter rodentium infection exacerbated pathology.

183 ion of NleB1, EPEC infection in vitro, or C. rodentium infection in vivo NleB overexpression resulted

184 C. rodentium infection induced IL-7 production from intesti

185 d by a deficit in ILC2s, whereas Citrobacter rodentium infection is cleared efficiently.

186 Citrobacter rodentium infection of mice induces cell-mediated immune

187 We examined the effects of C rodentium infection on control mice fed SCFAs and/or giv

188 owing microbiome disruption with Citrobacter rodentium infection or antibiotic treatment, suggesting

189 Importantly, transient C. rodentium infection protected IL-10-deficient mice again

190 ment with anti-IL-7Ralpha antibody during C. rodentium infection resulted in a higher bacterial burde

191 C. rodentium infection resulted in an altered fecal microbi

192 ased intestinal transport activity during C. rodentium infection results in fatality in C3H/HeOu and

193 C. rodentium infection strongly decreased guanylin expressi

194 infant mice are much more susceptible to C. rodentium infection than adult mice; infants infected wi

195 less able to eradicate a mucosal Citrobacter rodentium infection than wild-type C57BL/6 mice.

196 ype B. subtilis reduced disease caused by C. rodentium infection through a mechanism that required es

197 The pathogenesis of a Citrobacter rodentium infection was evaluated in mice fed diets with

198 ed morbidity and mortality after Citrobacter rodentium infection with decreased secretion of cytokine

199 During intestinal Citrobacter rodentium infection, a mouse model for enteropathogenic

200 at link for the investigation of Citrobacter rodentium infection, a mouse model for enteropathogenic

201 nsequently, these mice are susceptible to C. rodentium infection, and both exogenous IL-22 and IL-23

202 thelial cells after T. gondii or Citrobacter rodentium infection, but also maintained the homeostatic

203 , and had a slower immune response against C rodentium infection, clearing the bacteria more slowly.

204 IEC) mice efficiently controlled Citrobacter rodentium infection, IKKalpha(DeltaIEC) mice exhibited s

205 d mucosal innate immune responses against C. rodentium infection, manifested by reduced crypt hyperpl

206 During C. rodentium infection, NK cells were recruited to mucosal

207 test the effects of stressor exposure on C. rodentium infection, we exposed resistant mice to a prol

208 Using mouse model of Citrobacter rodentium infection, we investigated the role of PFOS on

209 Ahr-deficient mice succumbed to Citrobacter rodentium infection, whereas ectopic expression of IL-22

210 Cs had no impact on control of intestinal C. rodentium infection, whereas lack of all ILC3s partially

211 atory RelA/NF-kappaB response to Citrobacter rodentium infection, while Nfkb2(-/-) mice succumbed to

212 nic inflammation throughout the course of C. rodentium infection.

213 longed reduction in the overall burden of C. rodentium infection.

214 nhanced mucosal immunity against Citrobacter rodentium infection.

215 biome both in the absence and presence of C. rodentium infection.

216 ph nodes and were susceptible to Citrobactor rodentium infection.

217 and coexpressed with IL-23 after Citrobacter rodentium infection.

218 tinal IL-22, and the inability to control C. rodentium infection.

219 tran sodium sulfate treatment or Citrobacter rodentium infection.

220 elial derived ILK in response to Citrobacter rodentium infection.

221 rypt hyperplasia and/or colitis following C. rodentium infection.

222 elial cell proliferative responses during C. rodentium infection.

223 capable of protecting mice from Citrobacter rodentium infection.

224 F-kappaB in colonic crypts in response to C. rodentium infection.

225 was essential for the control of mucosal C. rodentium infection.

226 previously characterized for outcomes of C. rodentium infection.

227 ing both Helicobacter pylori and Citrobacter rodentium infection.

228 g bacteria and susceptibility to Citrobacter rodentium infection.

229 of DOCK2 for gastrointestinal immunity to C. rodentium infection.

230 at mice lacking DOCK2 were susceptible to C. rodentium infection.

231 e conferred by aerobic respiration during C. rodentium infection.

232 role in modulation of immune responses to C. rodentium infection.

233 ducers of the innate response to Citrobacter rodentium infection.

234 epeated exposure to ketamine and Citrobacter rodentium infection.

235 and Y471 play in host immune responses to C. rodentium infection.

236 elper cell, type 17 responses in Citrobacter rodentium infections are driven by concomitant bacterial

237 ex virus, Toxoplasma gondii, and Citrobacter rodentium infections.

238 Infection with Citrobacter rodentium initially was controlled by ILC3, followed by

239 Infection of mice with Citrobacter rodentium is a robust model to study bacterial pathogene

240 Citrobacter rodentium is an attaching and effacing mouse pathogen th

241 Citrobacter rodentium is an enteric bacterial pathogen of the mouse

242 Citrobacter rodentium is an enteric pathogen which attaches itself t

243 C. rodentium is used to model the human pathogens enterohem

244 ion with the intestinal pathogen Citrobacter rodentium, leading to impaired survival.

245 against a murine enteropathogen, Citrobacter rodentium, leading to the death of the animals.

246 In-frame mutations of C. rodentium lifA glucosyltransferase (CrGlM21) and proteas

247 The Citrobacter rodentium model mimics the pathogenesis of infectious co

248 cific knockout of NLRX1 within a Citrobacter rodentium model of colitis.

249 ion and disease phenotype in the Citrobacter rodentium model of murine infectious colitis.

250 h the dextran sodium sulfate and Citrobacter rodentium models of colitis, significantly increased num

251 ropathogenic E. coli (EPEC), and Citrobacter rodentium Moreover, Salmonella enterica strains encode u

252 C. rodentium NleB, EHEC NleB1, and SseK1 glycosylated host

253 C. rodentium NleB, EHEC NleB1, EPEC NleB1, and SseK2 glycos

254 n by the murine enteric pathogen Citrobacter rodentium of the family Enterobacteriacea.

255 was induced by administration of Citrobacter rodentium or dextran sulfate sodium (DSS) to transgenic

256 susceptibility to induction of colitis by C rodentium or DSS, and reduced survival times compared wi

257 infected with Escherichia coli, Citrobacter rodentium or Vibrio cholerae.

258 roduction, an inability to clear systemic C. rodentium, or increased pathogenicity.

259 sing the mouse-specific pathogen Citrobacter rodentium Our murine infant model is similar to EPEC inf

260 Importantly, wild-type C. rodentium out-competed the tir tyrosine mutants during m

261 ibited significant colitis in response to C. rodentium plus DBZ.

262 cluding increased mucosal colonization by C. rodentium, prolonged pathogen shedding, exaggerated cyto

263 inding between recombinant hCD98 and EPEC/C. rodentium proteins.

264 lts suggest that the host defense against C. rodentium requires epithelial PI3K activation to induce

265 th Anaplasma phagocytophilum and Citrobacter rodentium respectively, were used.

266 ext of intestinal infection with Citrobacter rodentium, resulting in preserved innate immunity.

267 ANR homologs of Vibrio cholerae, Citrobacter rodentium, Salmonella enterica and ETEC were capable of

268 eria including Escherichia coli, Citrobacter rodentium, Salmonella typhimurium, and Shigella flexneri

269 geny of C. rodentium and identified 1,585 C. rodentium-specific (without orthologues in EPEC or EHEC)

270 otection from reinfection associated with C. rodentium-specific IgG responses comparable to those in

271 C. rodentium specifically activated the Nlrp3 inflammasome

272 olated from infected mice revealed that a C. rodentium strain expressing Tir_Y451A/Y471A recruited si

273 chromosome and four plasmids harbored by C. rodentium strain ICC168.

274 We characterized Citrobacter rodentium strains bearing deletions in individual type I

275 triggering colonic crypt hyperplasia, the C. rodentium T3SS induced an excessive expansion of undiffe

276 ne glycosyltransferase NleB1 (NleB(CR) in C. rodentium) that modifies conserved arginine residues in

277 Here we used C. rodentium to investigate the different Tir signalling pa

278 During peak infection with C. rodentium, Tpl2(-/-) mice experienced greater bacterial

279 d with increased frequency and numbers of C. rodentium translocation out of the intestine.

280 Citrobacter rodentium uses a type III secretion system (T3SS) to ind

281 We conclude that C. rodentium uses its T3SS to induce histopathological lesi

282 ll as the related mouse pathogen Citrobacter rodentium, utilize a type III secretion system (T3SS) to

283 cilli physically displaced and attenuated C. rodentium virulence by H2O2-mediated suppression of the

284 C. rodentium was administered to both control and intestina

285 Susceptibility of Il22ra1(-/-) mice to C. rodentium was associated with preferential expansion and

286 IL-7 production from IECs in response to C. rodentium was dependent on gamma interferon (IFN-gamma)-

287 The ability of commensals to outcompete C. rodentium was determined, at least in part, by the capac

288 C. rodentium was first isolated by Barthold from an outbrea

289 The deep sequencing data revealed that C. rodentium was most abundantly associated with the cecal

290 Citrobacter rodentium was used as a Th17-inducing infection model, i

291 Citrobacter rodentium was used to model human Escherichia coli infec

292 attaching and effacing bacteria Citrobacter rodentium, we defined the mechanisms and contributions o

293 tion and humoral immune responses against C. rodentium were severely impaired in infected miR-155-def

294 on by the enteric mouse pathogen Citrobacter rodentium, which causes disease similar to the human pat

295 attaching and effacing pathogen Citrobacter rodentium, which colonizes primarily the surfaces of the

296 d to the extracellular bacterium Citrobacter rodentium, which induces a mixed Th1 and Th17 response.

297 thelium with the rodent pathogen Citrobacter rodentium, which models human infections with the attach

298 Analysis of the mechanisms revealed that C. rodentium wild type differentially influenced Rho GTPase

299 tinal epithelial monolayers and mice with C. rodentium wild type resulted in compromised epithelial b

300 e at the peak of the infection eliminated C. rodentium within 16 days.