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 is used to model the human pathogens entero

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

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

12 C. rodentium specifically activated the Nlrp3 inflammaso

13 C. rodentium was administered to both control and intest

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

56 defense against enteric infections caused by C. rodentium.

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

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

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

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

61 the epithelial barrier compromise induced by C. rodentium.

62 inflammatory response and disease induced by C. rodentium.

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

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

65 olonization of the gastrointestinal tract by C. rodentium.

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

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

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

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

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

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

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

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

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

75 ithelial cell proliferative responses during C. rodentium infection.

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

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

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

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

80 98 was sufficient for direct binding to EPEC/C. rodentium.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

156 The C. rodentium espB mutant exhibited reduced cell associat

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

179 51 and Y471 play in host immune responses to C. rodentium infection.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

221 3 required for survival after infection with C. rodentium, but CD103(+) cDCs dependent on the transcr

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

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

224 rovide enhanced protection to infection with C. rodentium.

225 aling protects mice following infection with C. rodentium.

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

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

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

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

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

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

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