ライフサイエンスコーパス: C. jejuni

1 C. jejuni 81-176 naturally lacks the fuc locus and is un

2 C. jejuni also activated the NLRP3 inflammasome in human

3 C. jejuni is capable of systemic invasion in the rabbit,

4 C. jejuni is known to produce capsular polysaccharide (C

5 C. jejuni lineages vary in host range and prevalence in

6 C. jejuni lipooligosaccharide (LOS) is a potent activato

7 C. jejuni NCTC11168 forms less biofilms in the presence

8 C. jejuni OMVs contained 16 N-linked glycoproteins, indi

9 C. jejuni OMVs possess cytotoxic activity and induce a h

10 C. jejuni possesses an extensive repertoire of carbohydr

11 C. jejuni regulates gene expression under various enviro

12 C. jejuni typically colonizes the gut, but a hypervirule

13 C. jejuni-induced bactericidal NO production was reduced

14 cteriosis isolates, comprising 2,207 (89.3%) C. jejuni isolates and 265 (10.7%) C. coli isolates.

15 ed the antimicrobial susceptibilities of 320 C. jejuni and 115 C. coli isolates obtained from feedlot

16 erent time periods and compared them with 42 C. jejuni isolates associated with sheep abortion during

17 Here, we analyzed 54 C. jejuni isolates collected from U.S. sheep abortions a

18 LST-characterised isolates, we sequenced 600 C. jejuni and C. coli isolates from various stages of po

19 The first outbreak involved 1,644 C. jejuni infections at 11 state correctional facilities

20 A C. jejuni addAB mutant demonstrated enhanced sensitivity

21 A C. jejuni transposon (Tn) mutant library was screened fo

22 tients, who previously developed GBS after a C. jejuni infection (n = 27) and controls (n = 26).

23 OMVs isolated from a C. jejuni 11168H cdtA mutant induced interleukin-8 (IL-8

24 To address this, we generated a C. jejuni transposon mutant library that is amenable to

25 arker) than the CCV in cells infected with a C. jejuni wild-type strain.

26 Additionally, C. jejuni clone SA was identified in raw milk, cattle fe

27 vailable mouse monoclonal antibodies against C. jejuni were investigated to construct direct, sandwic

28 s in understanding the mechanisms that allow C. jejuni to colonize the chicken gastrointestinal tract

29 he context of glycoengineering and may alter C. jejuni glycan-mediated structure-function interaction

30 Although C. jejuni can be transformed by C. jejuni-derived DNA, i

31 Altogether, C. jejuni was isolated from 7 of 15 (46.7%) bovine fecal

32 es and time of isolation, while the analyzed C. jejuni isolates were genetically diverse, suggesting

33 ampylobacter jejuni subsp. jejuni 81-176 and C. jejuni NCTC 11168, all of which had previously been s

34 roglodytis (33%), C. upsaliensis (7.7%), and C. jejuni/C. coli (2.6%).

35 uni, preferred the native N. gonorrhoeae and C. jejuni substrates, respectively.

36 est that in the gut of warm-blooded animals, C. jejuni depends on at least formate or hydrogen as don

37 -10 expression, an intriguing observation as C. jejuni FlaA is not a TLR5 agonist.

38 In contrast to NLRP3 activation by ATP, C. jejuni activation did not require priming of these ma

39 Furthermore, neutrophil depletion attenuated C. jejuni-induced crypt abscesses and intestinal inflamm

40 Importantly, sodium nitroprusside attenuated C. jejuni-induced colitis in Il10(-/-); Nod2(-/-) mice.

41 flagella-TLR5 driven pro-inflammatory axis, C. jejuni flagella instead promote an anti-inflammatory

42 At dairy B, C. jejuni was cultured from 9 of 26 (34.6%) bovine fecal

43 findings are of additional interest because C. jejuni utilizes the flagellum to export virulence pro

44 we studied LOS structural variation between C. jejuni strains associated with different ecological s

45 to effectively control infections caused by C. jejuni.

46 consumption of meat that was contaminated by C. jejuni during harvest.

47 se leads to secretion of an alpha-dextran by C. jejuni and that a secreted protease, Cj0511, is requi

48 Lipo-oligosaccharides (LOS), expressed by C. jejuni induce antibodies that cross-react with self-g

49 e use of enterobactin hydrolysis products by C. jejuni, Vibrio cholerae, and other bacteria with homo

50 Although C. jejuni can be transformed by C. jejuni-derived DNA, it is poorly transformed by the s

51 provide evidence for l-fucose utilization by C. jejuni.

52 ght into the molecular mechanism utilized by C. jejuni, and possibly other intestinal pathogens, to s

53 h throughput glycoproteomics to characterize C. jejuni JHH1 and identified 93 glycosylation sites, in

54 To mediate chemotaxis, C. jejuni and H. pylori combine basic chemotaxis signal

55 nd shows antibody is ineffective in clearing C. jejuni from the ceca within the production lifetime o

56 In contrast, C. jejuni isolates from Great Britain were genetically d

57 ion in both the OS and LA among 15 different C. jejuni isolates.

58 blockade of PI3K-gamma signaling diminished C. jejuni-induced intestinal inflammation, neutrophil ac

59 obe sequences from 1,713 genetically diverse C. jejuni and C. coli genomes, supported by RT-PCR testi

60 lack of insight into the mechanisms driving C. jejuni growth and survival within hosts and the envir

61 Genes preferentially expressed during C. jejuni infection were screened, and acs, cj1385, cj02

62 ystem was found to be required for efficient C. jejuni colonization of the chicken intestine.

63 ridization and culture assay showed enhanced C. jejuni invasion into the colon and mesenteric lymph n

64 haped laboratory, clinical and environmental C. jejuni and Campylobacter coli contained genetic chang

65 ficity of the protein N-glycosylation enzyme C. jejuni PglB was tested using a logical, synthetic arr

66 ped severe intestinal inflammation following C. jejuni infection, compared with Nod2(-/-) and Il10(-/

67 For C. jejuni, strains with the fuc locus possess a competit

68 100% for Shigella spp., 97.5% and 99.0% for C. jejuni and C. coli, and 100% and 99.7% for Shiga toxi

69 99.7% for Shigella spp., 97.2% and 98.4% for C. jejuni and C. coli, and 97.4% and 99.3% for Shiga tox

70 , 8 x 10(-6), and 3 x 10(-7) [corrected] for C. jejuni, Salmonella spp., and enteroviruses, respectiv

71 We compared culture for C. jejuni/C. coli, EIA (ProSpecT), and duplex PCR to dis

72 cids does not appear to be a determinant for C. jejuni during commensalism.

73 ative Microbial Risk Assessment was done for C. jejuni, Salmonella spp., and enteroviruses to estimat

74 Instead, secretion of CiaI was essential for C. jejuni to facilitate commensal colonization of the na

75 ce in dairy manure, while risk estimates for C. jejuni were not sensitive to any single variable.

76 ved in LOS biosynthesis and is important for C. jejuni virulence, as disruption of this gene and the

77 f a rapid and sensitive detection method for C. jejuni.

78 orrelated with possession of the pathway for C. jejuni RM1221 (fuc+) and 81116 (fuc-).

79 IA-positive samples were positive by PCR for C. jejuni/C. coli, but 27.6% were positive for non-jejun

80 tively, compared with the results of PCR for C. jejuni/C. coli.

81 dentified several loci that are required for C. jejuni efficient entry and survival within epithelial

82 DNA synthesis via RNR which is required for C. jejuni's growth.

83 s, cj1385, cj0259 seem to be responsible for C. jejuni invasion.

84 r, these results support a critical role for C. jejuni's helical morphology in enabling it to travers

85 ), whereas pigs were a negligible source for C. jejuni infections.

86 Formate, a primary energy source for C. jejuni, inhibits oxidase activity in other bacteria.

87 We found C. jejuni to be a potent inducer of human and murine DC

88 e identical structure purified directly from C. jejuni.

89 III secretion sequence and is secreted from C. jejuni through the flagellar type III secretion syste

90 Our results provide new insights into how C. jejuni responds and adapts to the cecal environment a

91 However, C. jejuni lacks the virulence-associated secretion syste

92 tinguishable from those of 123 (9.03%) human C. jejuni isolates (total, 1,361) in the CDC database, a

93 The mean probability of human C. jejuni isolates to originate from chickens was highes

94 reported the identification of hyperinvasive C. jejuni strains and created a number of transposon mut

95 evelopment of vaccines against hypervirulent C. jejuni.

96 uoroquinolone resistance reached to 35.4% in C. jejuni and 74.4% in C. coli, which are significantly

97 s study, we demonstrate that sialic acids in C. jejuni endotoxin enhance the rapid production of IFN-

98 ts and phase-variants, the cj0031c allele in C. jejuni strain NCTC11168 was demonstrated to specifica

99 407 cells in vitro The importance of Ape1 in C. jejuni biology makes it a good candidate as an antimi

100 Additionally, overexpression of arsB in C. jejuni 11168 resulted in a 16-fold increase in the MI

101 Inactivation of arsB in C. jejuni resulted in 8- and 4-fold reduction in the MIC

102 protein while CtsP is membrane associated in C. jejuni.

103 In certain environments, changes in C. jejuni morphology due to genetic heterogeneity may pr

104 Here, oxygen-dependent changes in C. jejuni physiology were studied at constant growth rat

105 high-level resistance to chloramphenicol in C. jejuni, using integrated genomic and proteomic analys

106 study, we investigated the role of cj1136 in C. jejuni virulence, lipooligosaccharide (LOS) biosynthe

107 ique Ent trilactone esterase Cee (Cj1376) in C. jejuni.

108 st abundant periplasmic c-type cytochrome in C. jejuni, as a novel and unexpected protein required fo

109 HtrA deletion in C. jejuni led to severe defects in E-cadherin cleavage,

110 This mechanism of DNA discrimination in C. jejuni is distinct from the DNA discrimination descri

111 that Cee is the sole trilactone esterase in C. jejuni.

112 se that modal repeat numbers have evolved in C. jejuni genomes due to molecular drivers associated wi

113 aspecies conservation of the target genes in C. jejuni and C. coli Rare instances of a lack of specif

114 A genome-wide association study (GWAS) in C. jejuni ST-21 and ST-45 complexes identified genetic e

115 rulence plasmid named pVir was identified in C. jejuni 81-176 and IA3902, but determining the role of

116 onization, and host-pathogen interactions in C. jejuni Therefore, changes in PG greatly impact the ph

117 s and other arsenic resistance mechanisms in C. jejuni have not been characterized.

118 are major contributors to microaerophily in C. jejuni; hemerythrins help prevent enzyme damage micro

119 Generation of a mutant in C. jejuni 81-176 by interruption of cj0256 resulted in t

120 not required to regulate flagellar number in C. jejuni.

121 ether non-canonical N-glycans are present in C. jejuni, we utilized high throughput glycoproteomics t

122 B, arsC2, and arsR3 in arsenic resistance in C. jejuni and found that arsB, but not the other two gen

123 ernative mechanism for arsenic resistance in C. jejuni and provide new insights into the adaptive mec

124 assage on calcofluor white (CFW) resulted in C. jejuni 81-176 isolates with morphology changes: eithe

125 ergy metabolism and microaerobic survival in C. jejuni.

126 system constitutes a LIV transport system in C. jejuni responsible for a high level of leucine acquis

127 vealing genetic variability of this trait in C. jejuni due to spontaneous DNA replication errors occu

128 nes required for efficient transformation in C. jejuni include those similar to components of type II

129 re gene with the highest p-distance value in C. jejuni was annotated in the reference genome as a put

130 Recent work in C. jejuni identified a gene encoding a novel phosphoetha

131 ptome of many different organisms, including C. jejuni; however, this technology has yet to be applie

132 Formate also significantly increased C. jejuni's growth, motility, and biofilm formation unde

133 tinal inflammation in response to intestinal C. jejuni infection.

134 oration of the carbohydrate sialic acid into C. jejuni lipooligosaccharides (LOS) is associated with

135 situation and will allow novel insights into C. jejuni pathogenic mechanisms.

136 cting and 80-fold increases in intracellular C. jejuni 11168H wild-type strain bacteria were observed

137 Herein, we aimed to investigate C. jejuni-mediated effects on dendritic cell (DC) immuni

138 populations and provides evidence that major C. jejuni lineages have distinct genotypes associated wi

139 This review explores mechanisms C. jejuni and H. pylori employ to control flagellar bios

140 tions neither is optimal for microaerophilic C. jejuni nor reflects the low-oxygen environment of the

141 In this model, C. jejuni successfully established infection and piglets

142 Most C. jejuni capsules are known to be decorated nonstoichio

143 lysis of the invasive ability of a nonmotile C. jejuni 11168H rpoN mutant in the VDC model system ind

144 ed in dissemination of FQ(R) C. coli but not C. jejuni.

145 We report novel C. jejuni factors essential throughout its life cycle.

146 D) of 150 colony forming unit (CFU)mL(-1) of C. jejuni in solution.

147 lude that CiaI contributes to the ability of C. jejuni to survive within epithelial cells.

148 infections result in significant amounts of C. jejuni present in the food supply to contribute to di

149 Proteomic analysis of C. jejuni 11168H OMVs identified 151 proteins, including

150 Here, we report a detailed analysis of C. jejuni fitness across models reflecting stages in its

151 PCR analysis of C. jejuni isolates from different animals hosts indicate

152 Furthermore, analysis of C. jejuni localization within the ceca of infected mice

153 with H. pylori RdxA, biochemical analysis of C. jejuni RdxA showed strong oxidase activity, with redu

154 Analysis of a vast array of C. jejuni mutants with defects in capsule formation, LPS

155 duced the commensal colonization capacity of C. jejuni 81-176 in chicks.

156 ighlight a hitherto unrecognized capacity of C. jejuni to use tetrathionate and thiosulphate in its e

157 The capsule of C. jejuni 81-176 has been shown to be required for serum

158 hypervirulent and rapidly expanding clone of C. jejuni recently emerged, which is able to translocate

159 variations in three structural components of C. jejuni LOS alter TLR4 activation and consequent monoc

160 Control of C. jejuni is a priority for the poultry industry but no

161 of the phosphoramidate moiety in the CPS of C. jejuni is unknown.

162 alternative for the coordinated delivery of C. jejuni proteins into host cells.

163 ience, Cincinnati, OH), for the detection of C. jejuni and C. coli in 485 patient stool samples.

164 e been developed for the direct detection of C. jejuni and C. coli in stool specimens.

165 rod protein, FlgG, and the lipid A domain of C. jejuni lipooligosaccharide with a pEtN residue.

166 with a couple of exceptions, the ecology of C. jejuni and C. coli differed, with the latter forming

167 Exposure of C. jejuni to pancreatic amylase promotes biofilm formati

168 nhydrases (CAs) are encoded in the genome of C. jejuni strain NCTC 11168 (Cj0229 and Cj0237).

169 logy models of the N-linked glycoproteome of C. jejuni This evaluation highlights the potential diver

170 ndescribed substrate that supports growth of C. jejuni and identified the genetic locus associated wi

171 eacts with superoxide, rescued the growth of C. jejuni cultured in the presence of deoxycholate.

172 More specifically, continuous growth of C. jejuni in deoxycholate was found to: 1) induce the pr

173 We recently found that growth of C. jejuni in medium with deoxycholate, a component of bi

174 essity of the pmf for motility and growth of C. jejuni.

175 CfrB, a homolog of C. jejuni NCTC 11168 Cj0444, shares approximately 34% of

176 says for the detection and identification of C. jejuni, C. coli, Salmonella, and Yersinia species and

177 y poor understanding of the immunobiology of C. jejuni infection.

178 s of infection, the adhesion and invasion of C. jejuni to eukaryotic cells.

179 ypeptidase Pgp1 essential for maintenance of C. jejuni helical shape was recently identified.

180 ives a unique insight into the mechanisms of C. jejuni disease in terms of host physiology and contri

181 lthough the specific molecular mechanisms of C. jejuni pathogenesis have not been characterized in de

182 Specifically, we show that modification of C. jejuni lipid A with pEtN results in increased recogni

183 some phase variable genes during passage of C. jejuni in chickens.

184 el to study determinants of pathogenicity of C. jejuni.

185 butor to the capnophilic growth phenotype of C. jejuni.

186 a suggest that the capsule polysaccharide of C. jejuni and the MeOPN modification modulate the host i

187 e related to the capsular polysaccharides of C. jejuni HS:4 is very remarkable, owing to the unique,

188 l shape and extended this to a wide range of C. jejuni and C. coli isolates.

189 mprovement was accompanied by a reduction of C. jejuni translocation into the colon and extraintestin

190 Instead, two regions of C. jejuni FlhG that are absent or significantly altered

191 understanding of the metabolic repertoire of C. jejuni and the role of metabolic diversity in Campylo

192 is required for the chemotactic response of C. jejuni to galactose, as shown using wild type, alleli

193 aluable tools for investigating the roles of C. jejuni cell surface glycoconjugates in host pathogen

194 n the reannotation of the genome sequence of C. jejuni isolate NCTC 11168, chosen as being present in

195 Following deep sequencing of C. jejuni mutants in the cecal outputs, several novel fa

196 Utilizing a series of C. jejuni isogenic mutants we found the major flagellin

197 There are 47 Penner serotypes of C. jejuni, 22 of which fall into complexes of related se

198 , these results indicate that sialylation of C. jejuni LOS increases DC activation and promotes subse

199 and in vivo of a highly pathogenic strain of C. jejuni.

200 We report the 2.1-A crystal structure of C. jejuni MOMP expressed in E. coli and a lower resoluti

201 for CeuE within the Fe(III) uptake system of C. jejuni, provide a molecular-level understanding of th

202 Here we report the complete transcriptome of C. jejuni during colonization of the chicken cecum and i

203 be applied to defining the transcriptome of C. jejuni during in vivo colonization of its natural hos

204 tial for their function in transformation of C. jejuni.

205 these analyses enhance our understanding of C. jejuni PG maturation and help to clarify how PG struc

206 te a direct role of luxS in the virulence of C. jejuni in two different animal hosts.

207 plays an important role in the virulence of C. jejuni using an in vivo model of natural disease.

208 , which has two major porins, OmpC and OmpF, C. jejuni has one, termed major outer membrane protein (

209 eltapatA and DeltapatB had minimal impact on C. jejuni growth and fitness under the conditions tested

210 C. coli, one additional E. faecium, and one C. jejuni also developed resistance when exposed to 0.25

211 her, formate might play a role in optimizing C. jejuni's adaptation to the oxygen-limited gastrointes

212 Like many competent organisms, C. jejuni restricts the DNA that can be used for transfo

213 are essential for DNA replication) in other C. jejuni genomes.

214 ucidation of similar pathways found in other C. jejuni strains and other pathogens.

215 nctate phenotype not observed with the other C. jejuni genes, and this phenotype was abolished by mut

216 Like many bacterial pathogens, C. jejuni assembles complex surface structures that inte

217 4 stool specimens had been culture positive (C. jejuni/coli [n = 51], Salmonella species [n = 42], Sh

218 e development of novel strategies to prevent C. jejuni colonization of food-producing animals or to t

219 ogy due to genetic heterogeneity may promote C. jejuni survival.

220 that exposure to pancreatic amylase protects C. jejuni from stress conditions in vitro, suggesting th

221 he single Thr-86-Ile mutation in GyrA, FQ(R) C. jejuni isolates had other mutations in GyrA in additi

222 Similarly, Mtz(r) C. jejuni was isolated after both in vitro and in vivo g

223 y Campylobacter-seronegative adults received C. jejuni strain 81-176 via oral inoculation of 10(5), 1

224 Kinetic studies with purified recombinant C. jejuni TsdA showed it to be a bifunctional tetrathion

225 A highly virulent, tetracycline-resistant C. jejuni clone (clone SA) has recently emerged in rumin

226 a highly pathogenic, tetracycline-resistant C. jejuni clone (named SA) has become the predominant ca

227 We have searched C. jejuni genome for homologues and found one candidate

228 straight morphology, representing the second C. jejuni gene affecting cell shape.

229 All rod-shaped C. jejuni Tn mutants and all rod-shaped laboratory, clin

230 N-beta responses to i.v.-injected sialylated C. jejuni.

231 in the increased pathogenicity of sialylated C. jejuni and may be key to the initiation of B cell-med

232 d greatly reduced phagocytosis of sialylated C. jejuni.

233 the amplified response of DCs to sialylated C. jejuni LOS is CD14 dependent.

234 ampylobacter coli (41 out of 45) and in some C. jejuni (8 out of 32) primary strains from various sou

235 A well-characterized outbreak strain, C. jejuni 81-176, was investigated using a volunteer exp

236 and annotation of the second poultry strain, C. jejuni strain S3.

237 Here we used an infant rabbit to study C. jejuni infection, which enables us to define several

238 In this study, C. jejuni arsP was expressed in Escherichia coli and sho

239 k involved eight confirmed and three suspect C. jejuni cases linked to consumption of commercial raw

240 tent Escherichia coli and the native system, C. jejuni, revealed that efficient glycosylation of glyc

241 the addition of the pEtN-glycan to a target C. jejuni protein.

242 In response to a low oxygen tension, C. jejuni increases the transcription and activity of th

243 frA, which was rarely observed in the tested C. jejuni strains.

244 nalyzed for Campylobacter species other than C. jejuni and C. coli using a filtration method and micr

245 Additionally, we found that C. jejuni FlhG influences FlhF GTPase activity, which ma

246 We hypothesized that C. jejuni must repair DNA damage caused by reactive oxyg

247 e from ruminants to humans and indicate that C. jejuni clone SA is an important threat to public heal

248 Our findings indicate that C. jejuni-induced PI3K-gamma signaling mediates neutroph

249 In this study, we report that C. jejuni infection of mouse macrophages induces upregul

250 Subsequently, we showed that C. jejuni 81-176 (wildtype) exhibited enhanced chemoattr

251 The C. jejuni invasion-related activation of the NLRP3 infla

252 However, little is known about the C. jejuni determinants that mediate these processes.

253 etween peptide and glycan substrates and the C. jejuni PglB offer new experimental information on sub

254 Further, we assessed the C. jejuni genes required for infection of the porcine ga

255 We explored how the C. jejuni flagellum is a versatile secretory organelle b

256 ansferase according to the annotation of the C. jejuni NCTC11168 genome.

257 A comparison of the C. jejuni requirements to colonize the mouse intestine w

258 nation of epithelial cells infected with the C. jejuni ciaI mutant revealed that the CCV were more fr

259 activation libraries were generated in three C. jejuni strains and the impact on fitness during chick

260 for fitness during in vitro growth in three C. jejuni strains, revealing that a large part of its ge

261 mmasome activation and likely contributes to C. jejuni-induced intestinal inflammation.

262 his is first study of functional immunity to C. jejuni in chicken and shows antibody is ineffective i

263 ologic development of protective immunity to C. jejuni, we assessed the ability of an initial infecti

264 strain differences in protective immunity to C. jejuni.

265 n has a primary role in acquired immunity to C. jejuni.

266 retreated with anti-IL-10R were resistant to C. jejuni-induced intestinal inflammation compared with

267 ctional role of B lymphocytes in response to C. jejuni in the chicken through depletion of the B lymp

268 gh intrinsic dendritic cell (DC) response to C. jejuni LOS through Toll-like receptor 4 (TLR4) activa

269 The DC response to C. jejuni LOS was highly variable between, but not withi

270 igger intestinal inflammation in response to C. jejuni.

271 High responsiveness to C. jejuni LOS by former GBS patients was evidenced by in

272 Intrinsic DC responsiveness to C. jejuni LOS was investigated first in 20 healthy contr

273 ility to highly regulate gene transcription, C. jejuni encodes few transcription factors and its geno

274 nd PCR-derived DNA can efficiently transform C. jejuni when only a subset of the CtsM sites are methy

275 ous recombination is sufficient to transform C. jejuni, whereas otherwise identical unmethylated DNA

276 DNA derived from a ctsM mutant transforms C. jejuni significantly less well than DNA derived from

277 those elicited by the helix-shaped wild-type C. jejuni and complemented strains.

278 ired for in vitro competition with wild-type C. jejuni but is dispensable for growth in monoculture.

279 ne operon) are widely distributed in various C. jejuni strains, suggesting that Campylobacter require

280 rends within this Tn library, and in various C. jejuni wild type strains, were compared and correlate

281 We identified the ability of both viable C. jejuni and purified flagellum to bind to Siglec-10, a

282 e ceca, the main site of colonisation, where C. jejuni persist to beyond commercial slaughter age, bu

283 this mouse model was used to define whether C. jejuni's characteristic helical shape plays a role in

284 While C. jejuni infection can be reproduced in vitro using int

285 While C. jejuni PglB (CjPglB) can transfer many diverse glycan

286 e blue with E. coli K12 and rose bengal with C. jejuni showed an enhancing effect.

287 C. jejuni received an initial challenge with C. jejuni CG8421 with rechallenge 3 months later.

288 Compared with C. jejuni NCTC 11168 and 81-176, a clone SA isolate (IA3

289 we infected human monocyte-derived DCs with C. jejuni to examine the production of key proinflammato

290 Il10(-/-);Rag2(-/-) mice were infected with C. jejuni (10(9) CFU/mouse).

291 Il10(-/-); Nod2(-/-) mice were infected with C. jejuni (10(9) colony-forming units/mouse) 24 hours af

292 Less than 1 in 1,000 persons infected with C. jejuni develop GBS, and the factors that determine GB

293 in chemokine induction in DCs infected with C. jejuni.

294 subjects underwent a primary infection with C. jejuni CG8421; 14 (93.3%) experienced campylobacterio

295 immunologic evidence of prior infection with C. jejuni received an initial challenge with C. jejuni C

296 e development of GBS after an infection with C. jejuni.

297 ll plasma membranes during interactions with C. jejuni OMVs.

298 rudescent infection following treatment with C. jejuni-sensitive antibiotics.

299 peats was detected for polyC/G tracts within C. jejuni genomes.

300 ur findings provide further evidence that WW C. jejuni subtypes show niche adaptation and may be impo