ライフサイエンスコーパス: rodentium

1 ating in response to a pathogen (Citrobacter rodentium).

2 B(hi) T cells, or infection with Citrobacter rodentium.

3 colitis by the mucosal pathogen, Citrobacter rodentium.

4 retory IgA (SIgA) following infection with C rodentium.

5 ith the EPEC-like mouse pathogen Citrobacter rodentium.

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

7 colonization resistance against Citrobacter rodentium.

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

9 attaching and effacing bacterium Citrobacter rodentium.

10 rance of the intestinal pathogen Citrobacter rodentium.

11 ILCs exacerbated infection with Citrobacter rodentium.

12 d abrogated STING-mediated IEC killing of C. rodentium.

13 infected with the enteropathogen Citrobacter rodentium.

14 the protective immunity against Citrobacter rodentium.

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

16 the colon during infection with Citrobacter rodentium.

17 enterica serovar Typhimurium and Citrobacter rodentium.

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

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

20 t tolerance of the mild pathogen Citrobacter rodentium.

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

22 s and death after infection with Citrobacter rodentium.

23 ) and the natural mouse pathogen Citrobacter rodentium.

24 dextran sulfate sodium (DSS) or Citrobacter rodentium.

25 coordination of host defenses to Citrobacter rodentium.

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

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

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

29 esion forming bacterial pathogens such as C. rodentium.

30 ses to intestinal infection with Citrobacter rodentium.

31 ttaching/effacing mouse pathogen Citrobacter rodentium.

32 depletion during infection with Citrobacter rodentium.

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

34 n intestinal bacterial pathogen, Citrobacter rodentium.

35 attaching-and-effacing pathogen Citrobacter rodentium.

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

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

38 by the model bacterial pathogen Citrobacter rodentium.

39 ense against enteric infections caused by C. rodentium.

40 c pathogens Escherichia coli and Citrobacter rodentium.

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

42 t early-life lethal infection by Citrobacter rodentium.

43 e anti-swarming activity against Citrobacter rodentium.

44 by the EPEC-like mouse pathogen Citrobacter rodentium.

45 ive infectious colitis caused by Citrobacter rodentium.

46 ide enhanced protection to infection with C. rodentium.

47 uring challenge with the colonic pathogen C. rodentium.

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

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

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

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

52 rohemorrhagic E. coli (EHEC) and Citrobacter rodentium, a murine model for EHEC.

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

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

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

56 Here we used Citrobacter rodentium, a pathogen that colonizes the colonic surface

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 able to alter IgA levels in vitro, as was F. rodentium alone.

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

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

64 Faecalibaculum rodentium, an Erysipelotrichaceae species, depleted its

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

66 Citrobacter rodentium and Escherichia coli O157 triggered similar Th

67 e colon of BT-11-treated mice in Citrobacter rodentium and IL-10(-/-) mouse models of colitis.

68 nic strains of the microbiota-Faecalibaculum rodentium and its human homologue, Holdemanella biformis

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

70 is bacillus Calmette-Guerin, and Citrobacter rodentium and of tumor growth in a syngeneic tumor model

71 monocytogenes, Escherichia coli, Citrobacter rodentium and Pseudomonas aeruginosa.

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

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

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

75 monocytogenes, Escherichia coli, Citrobacter rodentium, and Pseudomonas aeruginosa.

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

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

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

79 ine promotes virulence gene expression in C. rodentium Arginine is an important modulator of the host

80 oyed the natural murine pathogen Citrobacter rodentium as a model of EHEC virulence to investigate th

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

96 y the enteric bacterial pathogen Citrobacter rodentium by consuming amino acids, thus starving the in

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

98 control mice, but opsonization of cultured C rodentium by SIgA isolated from I-Ab(DeltaIEC) mice was

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

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

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

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

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

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

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

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

107 Serum and local TNF in CIA paws and C. rodentium colons were significantly increased in LACC1 K

108 intestinal damage, and failed to contain C. rodentium compared to controls.

109 ptible to enteric infection with Citrobacter rodentium compared to wild-type (WT) mice evidenced by m

110 IL-17R(-/-) mice, after reinfection with C. rodentium compared with wild-type mice.

111 b(DeltaIEC) mice died after infection with C rodentium, compared with none of the control mice.

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

113 ays 6 and 12 post-infection with Citrobacter rodentium (CR) and tended to decline at days 20-34.

114 Citrobacter rodentium (CR) promotes crypt hyperplasia and tumorigene

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

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

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

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

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

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

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

122 ansfer of 11 bacterial strains, including B. rodentium, enriched in Rnf5(-/-) mice, establishes anti-

123 h Gram-negative bacteria such as Citrobacter rodentium, Escherichia coli, or Pseudomonas aeruginosa m

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

125 C. rodentium exposure was shown to increase ILK expression

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

127 te sodium-treated mice with an isolate of F. rodentium (F.

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

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

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

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

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

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

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

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

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

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

138 attaching and effacing pathogen Citrobacter rodentium in these.

139 hogenesis of the murine pathogen Citrobacter rodentium In this work, we aimed to gain a better unders

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

141 7 agonist R848 or infection with Citrobacter rodentium in vivo.

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

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

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

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

146 th the STING ligand, 2,3-cGAMP, inhibited C. rodentium-induced colitis in vivo.

147 However, in mice with C rodentium-induced colitis, loss of MHCII reduces bacteri

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

149 phenotype and protects mice from Citrobacter rodentium-induced colitis.

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

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

152 4, and caspase-1 were hypersusceptible to C. rodentium-induced gastrointestinal inflammation.

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

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

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

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

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

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

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

160 Here, we demonstrate that C. rodentium induces a population of IL-17A(+) CD4(+) T cel

161 Citrobacter rodentium induces transmissible murine colonic hyperplas

162 Citrobacter rodentium induces transmissible murine colonic hyperplas

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

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

165 mmation and influenza A virus or Citrobacter rodentium infection along with metagenomics analyses, mu

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

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

168 ry source of luminal H(2)O(2) early after C. rodentium infection and is required for Ccp-dependent gr

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

170 L-22(+) cells in the colon 3 months after C. rodentium infection are CD4(+) T cells.

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

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

173 duce colitis or confer protection against C. rodentium infection due to suboptimal Th17 cell differen

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

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

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

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

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

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

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

181 mice with IL-23 during the early phase of C. rodentium infection rescued IL-22 production from group

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

183 C. rodentium infection resulted in an altered fecal microbi

184 C. rodentium infection strongly decreased guanylin expressi

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

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

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

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

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

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

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

192 a major source of IL-22 during secondary C. rodentium infection, even before the T-cell phase of the

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

194 At the peak of C. rodentium infection, increased arginine concentration in

195 a significant host protective role during C rodentium infection, independent of CGRP receptor signal

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

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

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

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

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

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

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

203 e colonic inflammation following Citrobacter rodentium infection.

204 g bacteria and susceptibility to Citrobacter rodentium infection.

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

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

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

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

209 ducers of the innate response to Citrobacter rodentium infection.

210 epeated exposure to ketamine and Citrobacter rodentium infection.

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

212 the role of CGRP receptor signaling during C rodentium infection.

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

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

215 nhanced mucosal immunity against Citrobacter rodentium infection.

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

217 ph nodes and were susceptible to Citrobactor rodentium infection.

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

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

220 tran sodium sulfate treatment or Citrobacter rodentium infection.

221 elial derived ILK in response to Citrobacter rodentium infection.

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

223 7A after in vitro activation and Citrobacter rodentium infection.

224 ing both Helicobacter pylori and Citrobacter rodentium infection.

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

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

227 C. rodentium injects type III secretion system effectors in

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

229 Citrobacter rodentium is an attaching and effacing mouse pathogen th

230 Citrobacter rodentium is an enteric bacterial pathogen of the mouse

231 Citrobacter rodentium is an enteric pathogen which attaches itself t

232 Citrobacter rodentium is an extracellular enteric mouse-specific pat

233 Citrobacter rodentium is known to induce IL-17(+) and IL-22(+) CD4(+

234 The source of arginine sensed by C. rodentium is not dietary.

235 aemorrhagic Escherichia coli and Citrobacter rodentium, its surrogate in a mouse infection model, sen

236 Following oral administration of Citrobacter rodentium, LACC1 knockout (KO) mice had more severe colo

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

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

239 SERT decreases LEE expression and reduces C. rodentium loads.

240 This collectively suggests that C. rodentium may induce CD4(+) T(RM) cells.

241 The Citrobacter rodentium model mimics the pathogenesis of infectious co

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

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

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

245 nt regulation of the LEE are conserved in C. rodentium Moreover, during infection, EutR is required f

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

247 The E. coli and Citrobacter rodentium NleB effectors, as well as the Salmonella ente

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

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

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

251 tive fitness of E. coli LF82 and Citrobacter rodentium only during inflammation.

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

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

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

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

256 ighting the intimate relationship between C. rodentium pathogenesis, metabolism and the gut microbiot

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

258 e the importance of EutR in vivo EHEC and C. rodentium possess the locus of enterocyte effacement (LE

259 ecifically, the transcriptome of in vitro C. rodentium-primed Th17 cells resembled that of Th17 cells

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

261 emales with the enteric pathogen Citrobacter rodentium protects dams and offspring against oral chall

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

263 mmunization of dams with heat-inactivated C. rodentium reduces pathogen loads and mortality in offspr

264 ased in B cells of IL-21R(-/-) mice after C. rodentium reinfection.

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 ckade IL-21 in vivo suppressed intestinal C. rodentium-specific IgA production as well as IgA(+)CD38(

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 We characterized Citrobacter rodentium strains bearing deletions in individual type I

274 e in glutathione production, and promoted C. rodentium survival in oxidative stress conditions.

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 e intestines upon infection with Citrobacter rodentium, the percentage of IgA(+)CD38(+)CD138(-) memor

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

290 Citrobacter rodentium was used to model human Escherichia coli infec

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

292 Using the enteric mouse pathogen, C. rodentium, we demonstrate that signaling via IL-36 recep

293 n screen in the enteric pathogen Citrobacter rodentium, we find that the bacterium requires amino aci

294 mmation and host defense against Citrobacter rodentium were not impaired in the absence of alpha4 int

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

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

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

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

299 ugments murine disease caused by Citrobacter rodentium, which is a murine pathogen extensively employ

300 d intimate epithelial attachment provides C. rodentium with oxygen for aerobic respiration.

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