ライフサイエンスコーパス: C. rodentium

1 C. rodentium activated DC especially in colon-draining L

2 C. rodentium espB was found to have 90% identity to EPEC

3 C. rodentium exposure was shown to increase ILK expressi

4 C. rodentium harbors two type VI secretion systems (T6SS

5 C. rodentium induces systemic T-cell-dependent antibody

6 C. rodentium infection induced IL-7 production from inte

7 C. rodentium infection resulted in an altered fecal micr

8 C. rodentium infection strongly decreased guanylin expre

9 C. rodentium injects type III secretion system effectors

10 C. rodentium is used to model the human pathogens entero

11 C. rodentium NleB, EHEC NleB1, and SseK1 glycosylated ho

12 C. rodentium NleB, EHEC NleB1, EPEC NleB1, and SseK2 gly

13 C. rodentium specifically activated the Nlrp3 inflammaso

14 C. rodentium was administered to both control and intest

15 C. rodentium was first isolated by Barthold from an outb

16 C. rodentium, which apparently infects only mice, provid

17 Here, we report the examination of 15 C. rodentium isolates using a battery of genetic and bio

18 ylogeny of C. rodentium and identified 1,585 C. rodentium-specific (without orthologues in EPEC or EH

19 isolated from infected mice revealed that a C. rodentium strain expressing Tir_Y451A/Y471A recruited

20 etically ablated (GC-C-/-) were administered C. rodentium by orogastric gavage and analyzed at multip

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

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

23 proves survival of IL-22 knockout mice after C. rodentium infection.

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

25 t IL-22(+) cells in the colon 3 months after C. rodentium infection are CD4(+) T cells.

26 antly greater antimicrobial activity against C. rodentium than those of mutant Cnlp-/- mice that lack

27 important regulator of host defense against C. rodentium by protecting the mucosa against ulceration

28 e results indicate that host defense against C. rodentium depends on B cells and IgG antibodies but d

29 flammasome signaling in host defense against C. rodentium has not been characterized.

30 Notably, the defective host defense against C. rodentium in Stat3(CD4) mice could be fully restored

31 esults suggest that the host defense against C. rodentium requires epithelial PI3K activation to indu

32 not only contribute to host defense against C. rodentium, but provide protection against infection-a

33 gnificant but modest role in defense against C. rodentium, whereas CXCR2 had a major and indispensabl

34 a-catenin signaling and host defense against C. rodentium.

35 e in the early phase of host defense against C. rodentium.

36 ii, it was required for host defense against C. rodentium.

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

38 +) cells during host defense in mice against C. rodentium.

39 induce colitis or confer protection against C. rodentium infection due to suboptimal Th17 cell diffe

40 ired mucosal innate immune responses against C. rodentium infection, manifested by reduced crypt hype

41 rmation and humoral immune responses against C. rodentium were severely impaired in infected miR-155-

42 d coadministration of probiotics ameliorated C. rodentium-induced barrier dysfunction, epithelial hyp

43 d protease that is critical for E. coli- and C. rodentium-induced inflammasome activation, but dispen

44 were introduced into EPEC strain CVD206 and C. rodentium strain DBS255, which both contain deletion

45 gate the importance of EutR in vivo EHEC and C. rodentium possess the locus of enterocyte effacement

46 However, NleB delivery during EPEC and C. rodentium infection caused rapid and preferential mod

47 the A/E lesion by both EPEC (Int(EPEC)) and C. rodentium (Int(CR)).

48 Serum and local TNF in CIA paws and C. rodentium colons were significantly increased in LACC

49 smotic diarrhea reduced colitis severity and C. rodentium burden in claudin-2-deficient, but not tran

50 at, in our hands, caused the same disease as C. rodentium.

51 g-lesion forming bacterial pathogens such as C. rodentium.

52 obacilli physically displaced and attenuated C. rodentium virulence by H2O2-mediated suppression of t

53 c-oxide (NO) synthase (iNOS) have attenuated C. rodentium-induced colitis.

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

55 Dead intimin beta+ C. rodentium, intimin alpha-transfected C. rodentium or

56 assess differences in pathogenicity between C. rodentium isolates from diverse sources.

57 ghlighting the intimate relationship between C. rodentium pathogenesis, metabolism and the gut microb

58 e, we report the detection of bioluminescent C. rodentium and commensal E. coli during colonization o

59 This correlated with inhibition of both C. rodentium-stimulated IkappaB-alpha phosphorylation an

60 redisposition to intestinal damage caused by C. rodentium but not to that caused by chemical irritant

61 d-type B. subtilis reduced disease caused by C. rodentium infection through a mechanism that required

62 osal hyperplasia identical to that caused by C. rodentium live infection, as well as a massive T help

63 defense against enteric infections caused by C. rodentium.

64 the intestinal epithelia to damage caused by C. rodentium.

65 including increased mucosal colonization by C. rodentium, prolonged pathogen shedding, exaggerated c

66 The mucosal changes elicited by C. rodentium were interferon-gamma-dependent.

67 -Mb chromosome and four plasmids harbored by C. rodentium strain ICC168.

68 t resistance and in the pathology induced by C. rodentium, an infection that mimics disease caused by

69 the epithelial barrier compromise induced by C. rodentium.

70 inflammatory response and disease induced by C. rodentium.

71 and colonization of the murine intestine by C. rodentium were also modulated by the modified intimin

72 n and for colonization of laboratory mice by C. rodentium.

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

74 olonization of the gastrointestinal tract by C. rodentium.

75 nguishable from the previously characterized C. rodentium isolate DBS100.

76 ort into the lumen, pIgR or J chain, cleared C. rodentium normally.

77 r dendritic cells, were impaired in clearing C. rodentium.

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

79 testinal IL-22, and the inability to control C. rodentium infection.

80 eta-glucuronidase inhibitor (GUSi) decreased C. rodentium's colonization of the GI tract, without mod

81 Notably, NleL-deficient C. rodentium triggered more IEC extrusion than did wild-

82 Correspondingly, the DeltananT C. rodentium strain was significantly impaired in its ab

83 During C. rodentium infection, NK cells were recruited to mucos

84 ired for the early induction of IL-22 during C. rodentium infection, and adaptive immunity is not ess

85 creased intestinal transport activity during C. rodentium infection results in fatality in C3H/HeOu a

86 eatment with anti-IL-7Ralpha antibody during C. rodentium infection resulted in a higher bacterial bu

87 ulation of these receptors on T-cells during C. rodentium infection.

88 tage conferred by aerobic respiration during C. rodentium infection.

89 ithelial cell proliferative responses during C. rodentium infection.

90 mice at the peak of the infection eliminated C. rodentium within 16 days.

91 o prolonged restraint significantly enhanced C. rodentium-induced infectious colitis in resistant mic

92 s, which may contribute to stressor-enhanced C. rodentium-induced infectious colitis.

93 t binding between recombinant hCD98 and EPEC/C. rodentium proteins.

94 98 was sufficient for direct binding to EPEC/C. rodentium.

95 c crypt hyperplasia and/or colitis following C. rodentium infection.

96 y to facilitate crypt regeneration following C. rodentium-induced pathogenesis.

97 Here, we show that following C. rodentium infection Il22(-/-) mice succumb due to deh

98 EC pathogenesis, lpf(cr) is not required for C. rodentium virulence in either the C3H/HeJ or C57BL/6

99 To determine if lifA/efa1 is required for C. rodentium-induced colonic pathology in vivo, three in

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

101 (EPS), and showed that it protects mice from C. rodentium-induced colitis by inducing anti-inflammato

102 e could protect IKKalpha(DeltaIEC) mice from C. rodentium-induced morbidity.

103 ficiency of Cyba resulted in protection from C. rodentium and L. monocytogenes infection.

104 ociated with a profound defect in generating C. rodentium-specific IgA(+) Ab-secreting cells.

105 longed colonization associated with a higher C. rodentium burden in gastrointestinal tissue and sprea

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

107 rdin, a positive regulator of complement, in C. rodentium-induced colitis.

108 ndent regulation of the LEE are conserved in C. rodentium Moreover, during infection, EutR is require

109 inine glycosyltransferase NleB1 (NleB(CR) in C. rodentium) that modifies conserved arginine residues

110 lls were found throughout expanded crypts in C. rodentium colitis.

111 dministration of 6% pectin or 4% curcumin in C. rodentium-infected mice also inhibited NF-kappaB acti

112 d a class 1 SPATE null mutant (Deltacrc1) in C. rodentium.

113 lysis reveal greater enterocyte depletion in C. rodentium-infected Il22(-/-) mice, resulting in signi

114 ne mechanisms of host defense and disease in C. rodentium infection.

115 ginine promotes virulence gene expression in C. rodentium Arginine is an important modulator of the h

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

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

118 nt stressor led to a significant increase in C. rodentium colonization over that in nonstressed contr

119 a host actin regulatory protein involved in C. rodentium and EHEC attachment to the gut epithelium v

120 A nonpolar insertion mutation in C. rodentium espB was constructed and used to replace th

121 Metabolic changes occur in C. rodentium-exposed ILC3s, but only trained ILC3s have

122 data indicate that arginase is protective in C. rodentium colitis by enhancing the generation of poly

123 eropathogenic E. coli effector repertoire in C. rodentium was not sufficient for efficient colonizati

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

125 n both the nucleus and the cytosol, while in C. rodentium-infected colon Foxo3a is expressed along th

126 d upstream of Y451 and downstream of Y471 in C. rodentium colonization and A/E lesion formation.

127 l immunization of dams with heat-inactivated C. rodentium reduces pathogen loads and mortality in off

128 erbated disease severity in both infectious (C. rodentium) and chemically induced (DSS) colitis, ampl

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

130 )ILCs had no impact on control of intestinal C. rodentium infection, whereas lack of all ILC3s partia

131 Blockade IL-21 in vivo suppressed intestinal C. rodentium-specific IgA production as well as IgA(+)CD

132 ells also have the capacity to directly kill C. rodentium.

133 lts demonstrate that MPEC is a misclassified C. rodentium isolate and that members of this species ar

134 Moreover, C. rodentium also sensed and displayed chemotactic activ

135 Moreover, C. rodentium-induced expansion and activation of intesti

136 ls, was essential for the control of mucosal C. rodentium infection.

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

138 result, sialic acid enhanced the ability of C. rodentium to degrade intestinal mucus (through Pic),

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

140 f colonic cells, increased the attachment of C. rodentium in mouse colons and resulted in increased e

141 prolonged reduction in the overall burden of C. rodentium infection.

142 beta-catenin signaling and the clearance of C. rodentium independent of adaptive immune responses.

143 olonic inflammation throughout the course of C. rodentium infection.

144 lucuronidase production led to a decrease of C. rodentium tissue colonization, compared to animals mo

145 termine the in vivo colonization dynamics of C. rodentium.

146 and abrogated STING-mediated IEC killing of C. rodentium.

147 These mice harbored increased levels of C. rodentium bacteria, showed more pronounced weight los

148 ient diet for 6 weeks had increased loads of C. rodentium in the colon and spleen, which were not obs

149 cence system and the colonic localization of C. rodentium, in vivo localization studies were performe

150 virulence to an intimin-deficient mutant of C. rodentium DBS255.

151 ry of signature-tagged transposon mutants of C. rodentium was constructed and screened in mice.

152 In-frame mutations of C. rodentium lifA glucosyltransferase (CrGlM21) and prot

153 ated with increased frequency and numbers of C. rodentium translocation out of the intestine.

154 een previously characterized for outcomes of C. rodentium infection.

155 The pathogenicity of C. rodentium DBS255 harbouring these plasmid derivatives

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

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

158 -) mice with IL-23 during the early phase of C. rodentium infection rescued IL-22 production from gro

159 ealed key information about the phylogeny of C. rodentium and identified 1,585 C. rodentium-specific

160 nes that encode the first described pilus of C. rodentium (named colonization factor Citrobacter, CFC

161 crobiome both in the absence and presence of C. rodentium infection.

162 ae could be accounted for by the presence of C. rodentium itself, which is a member of this family.

163 Production of C. rodentium antigen-specific IgM and IgG antibodies was

164 , we demonstrate that an avirulent strain of C. rodentium in the field has background mutations in ge

165 ificantly increased in the colonic tissue of C. rodentium-infected hCD98 Tg mice compared to that of

166 edia-linked apoE-mimetic peptide, COG112, on C. rodentium-activated cells.

167 To test the effects of stressor exposure on C. rodentium infection, we exposed resistant mice to a p

168 ession of NleB1, EPEC infection in vitro, or C. rodentium infection in vivo NleB overexpression resul

169 To address this question, we conducted oral C. rodentium infections in mice lacking B cells, IgA, se

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

171 , during challenge with the colonic pathogen C. rodentium.

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

173 were infected by oral gavage with pathogenic C. rodentium.

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

175 erized EPS and showed that they also prevent C. rodentium-associated intestinal disease after a singl

176 Mice infected with Stx-producing C. rodentium developed AE lesions on the intestinal epit

177 ease in glutathione production, and promoted C. rodentium survival in oxidative stress conditions.

178 ated intimate epithelial attachment provides C. rodentium with oxygen for aerobic respiration.

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

180 ng SERT decreases LEE expression and reduces C. rodentium loads.

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

182 herichia coli (EPEC and EHEC, respectively), C. rodentium exploits a type III secretion system (T3SS)

183 R are unable to clear Citrobacter rodentium (C. rodentium) but are protected from DSS-induced colitis

184 cterial burden during Citrobacter rodentium (C. rodentium) infection in mice.

185 E) and susceptible to Citrobacter rodentium (C. rodentium) infection.

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

187 In this study, C. rodentium espB has been cloned and its nucleotide seq

188 e production, an inability to clear systemic C. rodentium, or increased pathogenicity.

189 cess to a common pool of mobile DNA and that C. rodentium has lost gene functions associated with a p

190 We conclude that C. rodentium uses its T3SS to induce histopathological l

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

192 We previously found that C. rodentium lacking Rnr exhibits prolonged shedding and

193 ed the intestinal mucus layer, we found that C. rodentium was able to catabolize sialic acid, a monos

194 In addition, BLI revealed that C. rodentium colonizes the rectum, a site previously unr

195 The deep sequencing data revealed that C. rodentium was most abundantly associated with the cec

196 Analysis of the mechanisms revealed that C. rodentium wild type differentially influenced Rho GTP

197 These results show that C. rodentium infection provides a relevant, simple, and

198 Our findings suggest that C. rodentium has evolved to express a complex network of

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

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

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

202 The C. rodentium espB mutant also failed to colonize laborat

203 The C. rodentium espB mutant exhibited reduced cell associat

204 by triggering colonic crypt hyperplasia, the C. rodentium T3SS induced an excessive expansion of undi

205 COG112 inhibited the C. rodentium-stimulated induction of iNOS and the CXC ch

206 This in vivo screen revealed that the C. rodentium type I-E CRISPR system is required to suppr

207 tion were protected from disease even though C. rodentium colonization was not inhibited.

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

209 lrc4, and caspase-1 were hypersusceptible to C. rodentium-induced gastrointestinal inflammation.

210 IFN-gamma activated the mucosal immunity to C. rodentium infection by increasing the expression of i

211 le of DOCK2 for gastrointestinal immunity to C. rodentium infection.

212 Consistent with weakened innate immunity to C. rodentium, IKKalpha(DeltaIEC) mice displayed impaired

213 ion by ILC3s and impaired innate immunity to C. rodentium.

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

215 lained the sensitivity of Cxcr6(-/-) mice to C. rodentium.

216 istration of fucosylated oligosaccharides to C. rodentium-challenged Il22ra1(-/-) mice attenuated inf

217 ILK influences the host response to C. rodentium -induced infection, independently of reduce

218 agocytic cells, produced CCL2 in response to C. rodentium in a Nod2-dependent manner.

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

220 f NF-kappaB in colonic crypts in response to C. rodentium infection.

221 enhanced amount of TNF-alpha in response to C. rodentium infection.

222 exhibited significant colitis in response to C. rodentium plus DBZ.

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

224 much is known about the adaptive response to C. rodentium, the role of the innate immune response rem

225 the observed alterations in the response to C. rodentium.

226 histocompatibility complex II in response to C. rodentium.

227 ct role in modulation of immune responses to C. rodentium infection.

228 51 and Y471 play in host immune responses to C. rodentium infection.

229 Applying InducTn-seq to C. rodentium in a mouse model of infectious colitis bypa

230 eneration and tissue physiology similarly to C. rodentium-infected Il22(+/+) mice.

231 rodentium This heightened susceptibility to C. rodentium infection was ameliorated by RA supplementa

232 duce the stressor-enhanced susceptibility to C. rodentium-enhanced infectious colitis.

233 mice lacking DOCK2 were more susceptible to C. rodentium attachment to intestinal epithelial cells.

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

235 Consequently, these mice are susceptible to C. rodentium infection, and both exogenous IL-22 and IL-

236 to date have been found to be susceptible to C. rodentium infection.

237 that mice lacking DOCK2 were susceptible to C. rodentium infection.

238 nder a resistant mouse highly susceptible to C. rodentium.

239 eta+ C. rodentium, intimin alpha-transfected C. rodentium or E. coli strain K12, and EPEC induced muc

240 Importantly, transient C. rodentium infection protected IL-10-deficient mice ag

241 tigation showed that although both wild-type C. rodentium and DBS255(pCVD438) colonized the descendin

242 ctural examination of tissues from wild-type C. rodentium and DBS255(pCVD438)-infected mice revealed

243 iarrhoea following infections with wild-type C. rodentium compared with C. rodentiumDeltamap.

244 Mice challenged with wild-type C. rodentium develop a mucosal immunoglobulin A response

245 Following infection with wild-type C. rodentium IRTKS, but not IRSp53, was recruited to the

246 iving mice, challenged with either wild-type C. rodentium or DBS255(pCVD438), developed a mucosal imm

247 Importantly, wild-type C. rodentium out-competed the tir tyrosine mutants durin

248 C3H/HeJ mice were infected with a wild-type C. rodentium strain and its lpfA(cr) isogenic mutant.

249 ggered more IEC extrusion than did wild-type C. rodentium, resulting in diminished colonization of th

250 In contrast to infection with wild-type C. rodentium, that with any of the lifA/efa1 mutant stra

251 olonic epithelial cells and macrophages upon C. rodentium infection and was required for effective ho

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

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

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

255 symptomatic carriage of genetically virulent C. rodentium provided immune resistance against subseque

256 gainst the pathogen, phenotypically virulent C. rodentium, accumulated and infected the epithelium an

257 e immune system selectively targets virulent C. rodentium in the intestinal lumen to promote pathogen

258 specifically, the transcriptome of in vitro C. rodentium-primed Th17 cells resembled that of Th17 ce

259 ted Min mice were in the distal colon, where C. rodentium-induced hyperplasia occurs.

260 While C. rodentium injects into the host cells a second effect

261 With C. rodentium, COG112 improved the clinical parameters of

262 protection from reinfection associated with C. rodentium-specific IgG responses comparable to those

263 restraint stressor prior to a challenge with C. rodentium alters the intestinal microbiota community

264 the colonic microbiota during challenge with C. rodentium, and that these effects are long-lasting an

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

266 utive days and all mice were challenged with C. rodentium immediately following the first exposure to

267 adult and neonatal mice were challenged with C. rodentium, and a probiotic mixture containing Lactoba

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

269 Min mice infected with C. rodentium at 1 month of age were found to have a 4-fo

270 Mice infected with C. rodentium develop a secretory immunoglobulin A (IgA)

271 enterocytes isolated from mice infected with C. rodentium expressing Tir_Y451A/Y471A expressed signif

272 amin D-deficient diet and then infected with C. rodentium.

273 ells were more susceptible to infection with C. rodentium and showed increased bacterial disseminatio

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

275 s upregulated on day 12 after infection with C. rodentium in mice fed the doubly deficient diet compa

276 ILFs and host defense against infection with C. rodentium in mice lacking lymphotoxin signals, which

277 gher mortality rate following infection with C. rodentium than do wild-type animals.

278 3 required for survival after infection with C. rodentium, but CD103(+) cDCs dependent on the transcr

279 he production of IL-22 during infection with C. rodentium, but the lymphotoxin-like protein LIGHT did

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

281 aling protects mice following infection with C. rodentium.

282 than Cnlp+/+ mice after oral infection with C. rodentium.

283 rovide enhanced protection to infection with C. rodentium.

284 ice were protected from oral infections with C. rodentium inocula that infected the majority of Cnlp-

285 n before or 12 h after oral inoculation with C. rodentium, caused highly significant attenuation of i

286 Infection of mice with C. rodentium causes a breach of the intestinal epithelia

287 Infection of mice with C. rodentium causes breach of the colonic epithelial bar

288 Infection of laboratory mice with C. rodentium provides a useful in-vivo model for studyin

289 testinal epithelial monolayers and mice with C. rodentium wild type resulted in compromised epithelia

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