ライフサイエンスコーパス: H. pylori

1 H. pylori arsRS encodes a 2-component system critical fo

2 H. pylori bacterial load correlated positively with inte

3 H. pylori binding induces CEACAM1-mediated signalling, a

4 H. pylori cagY sequence differences and cagT4SS function

5 H. pylori eradication was assessed by UBT 6-10 weeks aft

6 H. pylori infection has been associated with the introdu

7 H. pylori infection increases DNA damage levels and lead

8 H. pylori proteins interfere with multiple host pathways

9 H. pylori strains can switch bg preference with single D

10 H. pylori tlpC mutants are outcompeted by wild type duri

11 H. pylori upregulates the expression and activity of sev

12 rized the cagA promoter and expression in 46 H. pylori strains from Portugal.

13 nucleotide polymorphism-based analysis of 63 H. pylori genomes again showed comparable phylogenetic c

14 HtrA presence was confirmed in 992 H. pylori isolates in gastric biopsy material from infec

15 ine kinase EGFR and the kinase Src abrogated H. pylori-induced MMP10 expression.

16 In addition, H. pylori eradication is not always beneficial as it has

17 ts, suggesting the involvement of additional H. pylori activities in mitochondria-mediated effects.

18 rent populations, which may yield additional H. pylori phenotypes.

19 moter was active specifically in AGS-adhered H. pylori, and this motif might be associated with high

20 In AGS cell-adhered H. pylori, it has a role in upregulation of cagA express

21 els to examine host determinants that affect H. pylori BabA expression.

22 sk of gastric cancer (GC) remains even after H. pylori eradication; thus, other combination treatment

23 in achieving good in vitro activity against H. pylori, having a MIC value of 4 mug/mL.

24 All H. pylori-challenged mice were successfully colonized.

25 that is geared towards find and destroy all H. pylori.

26 Multivariate analyses among H. pylori virulence genes and severity of hepatobiliary

27 iron deficiency may attenuate disease among H. pylori-infected persons with no response to antibioti

28 Furthermore, among H. pylori-infected children, those with a CagA+ strain h

29 elical parameters and flagellum number among H. pylori strains leading to distinct and broad speed di

30 ted with increased gastric cancer risk among H. pylori-infected persons.

31 An H. pylori constituent that augments cancer risk is the s

32 We determined that lactate is an H. pylori chemoattractant that is sensed via TlpC with a

33 Screening of an H. pylori transposon mutant library revealed that pro-IL

34 Infection of Mongolian gerbils with an H. pylori pgdA(-) mutant strain led to significantly dec

35 In longitudinal analyses, H. pylori infection at age 3 was inversely associated wi

36 We analyzed H. pylori strains isolated from Mongolian gerbils fed ei

37 scriptionally active microbial community and H. pylori gene expression were determined using metatran

38 role of NO in H. pylori-related diseases and H. pylori gene expression, and the mechanisms whereby H.

39 enterohepatic helicobacter species (EHS) and H. pylori These include flagellin, gamma-glutamyl transp

40 In total, 327 patients with GU and H. pylori infection (136 with IM and 191 without IM) wer

41 to 2.11 and 226 nM against S. pasteurii and H. pylori enzymes, respectively, indicating ebselen as o

42 tween BMI or obesity genetic risk scores and H. pylori positivity.

43 were analysed for total IgE levels and anti-H. pylori cytotoxin-associated gene A (CagA) IgG antibod

44 al data revealed no association between anti-H. pylori IgG titer and BMI, nor of H. pylori positivity

45 onamide inhibitors of HpalphaCA possess anti-H. pylori activity.

46 s but also in most individuals classified as H. pylori uninfected using conventional methods.

47 derrepresented, in gastric cancer-associated H. pylori isolates worldwide.

48 from human gastric organoids rapidly attract H. pylori.

49 To evaluate the stability of augmented H. pylori virulence phenotypes stimulated by low-iron co

50 Like other bacteria, H. pylori uses chemoreceptors and conserved chemotaxis p

51 or a clinically relevant association between H. pylori and BMI/obesity.

52 studies to quantify the association between H. pylori infection and atopy.

53 We examined associations between H. pylori infection in early childhood and atopy and rep

54 We found no associations between H. pylori seropositivity overall either by whole-cell EL

55 e performed to test for correlations between H. pylori strain properties and microbiota composition.

56 compare the difference in GU healing between H. pylori-infected patients with IM and those without IM

57 To establish a tight interaction between H. pylori and epithelial cells, the bacterium produces a

58 domization showed no causal relation between H. pylori genetic risk score and BMI/obesity, nor betwee

59 Here, we examine the relationship between H. pylori colonization and BMI/obesity.

60 g an intermediate evolutionary stage between H. pylori from European and East Asian countries.

61 MMP10 in gastric epithelial cells induced by H. pylori Infection of gastric cells with H. pylori led

62 ligomerizing mutant form of VacA secreted by H. pylori The nonoligomerizing 88-kDa mutant protein ret

63 P3 as well as induction of TLR2 signaling by H. pylori.

64 Lactate is utilised by H. pylori, and our work suggests that this pathogen seek

65 e majority of persons colonized with CagA(+) H. pylori strains do not develop cancer, suggesting that

66 During colonization, H. pylori uses motility and its chemotaxis signalling sy

67 promising novel therapeutic target to combat H. pylori-associated diseases.

68 In conclusion, H. pylori infection was associated with a significant in

69 henotypes stimulated by low-iron conditions, H. pylori isolated from iron-depleted conditions in vivo

70 In cross-sectional analysis, current H. pylori infection at age 6.5 years was inversely, thou

71 inases abolished and significantly decreased H. pylori-induced MMP10 expression, respectively, wherea

72 ureB-deficient H. pylori mutants were defective for CASP1 activation in

73 lial cells with wild-type and VacA-deficient H. pylori strains, treatment of cells with purified VacA

74 ltacrdS) and crdR/crdS-knockout (DeltacrdRS) H. pylori, but not arsS-knockout (DeltaarsS) or fleS-kno

75 rofiling analysis of wild-type and DeltacrdS H. pylori in the presence or absence of NO showed that 1

76 out (DeltaarsS) or fleS-knockout (DeltafleS) H. pylori, showed a significant loss of viability upon e

77 to uninfected animals (independent of diet), H. pylori-infected gerbils had significantly lower hemog

78 sy specimens from individuals with different H. pylori infection statuses and premalignant tissue cha

79 IL-18 is required for Treg differentiation, H. pylori persistence, and protection against allergic a

80 These processes generate diverse H. pylori subpopulations, in which BabA's adaptive evolu

81 lated in murine and human macrophages during H. pylori infection.

82 IL-10 neutralization during H. pylori infection led to increased IL-17-mediated resp

83 Mongolian gerbils (either H. pylori infected or uninfected) received a normal diet

84 based on genetic loci associated with either H. pylori colonization or BMI/obesity.

85 monstrate that CrdR-crdA interaction enables H. pylori to survive under nitrosative stress.

86 nt mice were inefficient in killing engulfed H. pylori Furthermore, recombinant Gal3 not only induced

87 As expected, H. pylori-infected MMP7(-/-) C57BL/6 mice exhibited a si

88 in individuals who had cleared experimental H. pylori infection compared with those who had not.

89 We hypothesize that these changes favor H. pylori persistence and disease.

90 Stool samples were analysed for H. pylori antigen using a rapid immunochromatographic te

91 Both for H. pylori and H. suis, it has been hypothesized that the

92 antly composed of T cells, mainly CD4(+) for H. pylori and CD8(+) for H. felis.

93 10(0), 10(2), and 10(2) bacterial cells for H. pylori detection and two different SNP sites strains.

94 Biopsy samples were tested for H. pylori using a reused Pronto Dry test, a reused CLOte

95 pared the efficacy of sequential therapy for H. pylori eradication exclusively in inactive duodenal u

96 Antibiotic treatment for H. pylori infections is challenging as drug resistance h

97 cal-junctional complexes, paving the way for H. pylori to access the basolateral compartment and trig

98 Compelling human in vivo data from H. pylori-positive gastritis tissues indicated that the

99 o-IL-1beta expression is induced by LPS from H. pylori, while the urease B subunit (UreB) is required

100 -producing leukocytes, biopsy specimens from H. pylori-infected patients, controls, and participants

101 extracted from 294 raw stool specimens from H. pylori-positive and -negative patients.

102 Furthermore, H. pylori abundance is positively correlated with the pr

103 type mice resulted in a reduction of gastric H. pylori colonization compared with nontreated mice.

104 In comparison to uninfected gerbils, H. pylori-infected gerbils had a higher gastric pH, a hi

105 treatments, it is crucial to understand how H. pylori is able to sense its niche for chronic infecti

106 OS(+) PCs are induced in the course of human H. pylori infection, and their abundance seems to correl

107 The "Iceman" H. pylori is a nearly pure representative of the bacteri

108 was found in prophages in contrast to 39% in H. pylori genome.

109 hohydrolase that triggers RNA degradation in H. pylori, whereas the other, HP0507, lacks such activit

110 rtion sequences (IS) previously described in H. pylori.

111 tion, as well as a possible role of diet, in H. pylori-associated IDA.

112 unveil two novel mitochondrial effectors in H. pylori-host interaction with links on gastric pathoge

113 al analysis showed that IL-17C expression in H. pylori-infected gastric biopsy specimens was predomin

114 NA was upregulated approximately 4.5-fold in H. pylori-infected gastric biopsy specimens.

115 ylogenetic analysis of 28 prophages found in H. pylori isolates from patients of distinct disease typ

116 MMP-10 may be implicated in H. pylori-mediated extracellular matrix remodeling.

117 s gastric mucosal neutrophil infiltration in H. pylori-infected Le(b)-expressing mice, providing pers

118 t the SAXS data suggested that the linker in H. pylori MotB forms a subdomain between the plug and th

119 ferritin values were significantly lower in H. pylori-infected gerbils than in uninfected gerbils, c

120 and showed that phase variation of modH5 in H. pylori P12 influenced expression of motility-associat

121 sues and epithelial cells, the role of NO in H. pylori-related diseases and H. pylori gene expression

122 recent findings on the expression of NOS2 in H. pylori-infected gastric tissues and epithelial cells,

123 We wanted to elucidate the status of Noxa in H. pylori-infected GECs.

124 obacter species and their occurrence only in H. pylori and close relatives provide a target for devel

125 s of IL-17 family cytokines was performed in H. pylori-infected and uninfected gastric biopsy specime

126 PCs) as one major iNOS(+) cell population in H. pylori-infected patients and confirmed intracellular

127 rapid detection of antibiotic resistance in H. pylori.

128 evasion, and loss of cell junctions seen in H. pylori-infected host cells.

129 lammation and associated oxidative stress in H. pylori-infected animals and that these conditions, al

130 This motif is vastly underrepresented in H. pylori genomes, but overrepresented in a number of vi

131 Different virulence factors, including H. pylori gamma-glutamyltranspeptidase (gGT), have been

132 oid cells attenuated gastritis and increased H. pylori burden in infected mice.

133 one of three diets associated with increased H. pylori virulence: high-salt, low-iron, or a combinati

134 xamination plus rapid urease test indicating H. pylori infection; 2) gastric IM adjacent to a GU but

135 In HIV-negative individuals, H. pylori infection was associated with decreased freque

136 mouse model of H. pylori-induced infection, H. pylori was specifically detected through both T2-weig

137 We next inoculated H. pylori Sydney strain 1 into wild-type (WT) and Gal3-d

138 and characterized a large panel of isogenic H. pylori strains that differ primarily in the CagA EPIY

139 We sequentially isolated H. pylori (strain J99) from a patient who developed corp

140 inhibitor is sufficient to effectively kill H. pylori, but not other bacteria.

141 the harsh environment of the stomach lumen, H. pylori colonizes the mucosal surface and within the g

142 nsistent with findings in the C57BL/6 model, H. pylori-infected MMP7-deficient INS-GAS mice exhibited

143 stent with Bhutanese strains having multiple H. pylori virulence factors associated with an increase

144 eater among cagA-positive than cagA-negative H. pylori infections (P = 0.012).

145 Hypersegmentation requires direct neutrophil-H. pylori contact as well as transcription and both host

146 As a consequence, 10 new H. pylori antibiotic candidates are identified, all of w

147 For patients with no H. pylori resistance to CLARI, a history of frequent inf

148 Even for cases with no H. pylori resistance to the used antibiotics, results we

149 Consistent with these observations, H. pylori infection increases stromal R-spondin 3 expres

150 t Gal3 not only induced rapid aggregation of H. pylori but also exerted a potent bactericidal effect

151 orted here are transition-state analogues of H. pylori MTAN with dissociation constants of 50 pM or b

152 In parallel, analyses of H. pylori status, carriage of the cag pathogenicity isla

153 e cag pathogenicity island and assignment of H. pylori to phylogeographic groups were performed to te

154 Coculture of H. pylori strain 7.13 or its pgdA(-) isogenic mutant wit

155 te immunity to infection and colonization of H. pylori.

156 he risk for malignancy within the context of H. pylori infection and provide an important framework f

157 There was no significant correlation of H. pylori phylogeographic population or carriage of the

158 this work and participated in the design of H. pylori infection studies, was inadvertently omitted f

159 However, detection of H. pylori infection at any point up to age 6.5 years was

160 d direct method for the in situ detection of H. pylori remains a challenge, mainly due to the strong

161 agnetic resonance imaging (MRI) detection of H. pylori.

162 imal models to accelerate the development of H. pylori-induced precancerous lesions.

163 investigated whether the diversification of H. pylori is influenced by the composition of the diet.

164 urrent study, we have analyzed the effect of H. pylori gGT on human DCs and the subsequent adaptive i

165 us, the current study analyzed the effect of H. pylori infection on the DNA damage response sensor, A

166 ogic assays confirmed a protective effect of H. pylori.

167 The independent effects of H. pylori infection (measured at age of 3, 5 and 6.5 yea

168 , the least characterized mobile elements of H. pylori.

169 SMOX-mediated DNA damage in the etiology of H. pylori-associated gastric cancer.

170 regression analysis revealed that failure of H. pylori eradication (Odds = 4.013, 95% CI: 1.840-8.951

171 Motility and the number of flagella of H. pylori P12 wild-type were significantly higher than t

172 inst allergic asthma, which is a hallmark of H. pylori-infected mice and humans.

173 efulness of this concept by modeling HPIs of H. pylori to understand how they modulate host immunity,

174 this study was to investigate the impact of H. pylori infection on markers of T-cell activation in H

175 hat contribute to maintaining high levels of H. pylori loads in the stomach by modulating effector T

176 We now demonstrate that levels of H. pylori-mediated TLR9 activation and expression are di

177 In a mouse model of H. pylori-induced infection, H. pylori was specifically

178 een anti-H. pylori IgG titer and BMI, nor of H. pylori positivity and BMI.

179 The role of IL-17C in the pathogenesis of H. pylori-induced diseases remains to be determined.

180 demonstrated a clear birth-cohort pattern of H. pylori infection in the Japanese population.

181 st environment on the virulence phenotype of H. pylori to understand how only a subset of infected in

182 ggest a possible basis for the phenotypes of H. pylori mutants lacking this enzyme.

183 The extant European population of H. pylori is known to be a hybrid between Asian and Afri

184 ification was used to detect the presence of H. pylori as well as to predict the phenotype of the org

185 sing stool samples to detect the presence of H. pylori DNA while concurrently detecting mutations ass

186 PCR-based assays for determining presence of H. pylori infection and two DNA single-point mutation as

187 w of studies that reported the prevalence of H. pylori infection among Japanese individuals.

188 count for heterogeneity in the prevalence of H. pylori infection as a function of birth year.

189 The decreased prevalence of H. pylori infection in successive generations should be

190 Changing trends in the prevalence of H. pylori infection in the general population over time

191 However, whether the prevalence of H. pylori infection itself shows a birth-cohort pattern

192 The prevalence of H. pylori infection was higher in O. viverrini-infected

193 y may contribute to the varied prevalence of H. pylori-related gastric cancer observed in diverse pop

194 ion molecule (CEACAM) family as receptors of H. pylori and show that HopQ is the surface-exposed adhe

195 and how it mediates epigenetic regulation of H. pylori motility.

196 was used to investigate a potential role of H. pylori infection, as well as a possible role of diet,

197 ; therefore, we sought to define the role of H. pylori PgdA in NOD1-dependent activation of NF-kappaB

198 ons of sodium chloride, lead to selection of H. pylori strains that are most fit for growth in this e

199 The sensitivity of H. pylori detection by PCR was 93.8%.

200 iet influences the incidence and severity of H. pylori-induced IDA.

201 Similarly, in the stomachs of H. pylori-infected patients, the human SLFN4 ortholog SL

202 an infection with a more virulent strain of H. pylori.

203 nfected with a more virulent CagA+ strain of H. pylori.

204 astric epithelial cells, clinical strains of H. pylori from the high-risk region induced more SMOX ex

205 pathogenically significant cagA+ strains of H. pylori Notably, we found that SOX9 was required for b

206 Here, we present a 5300-year-old H. pylori genome from a European Copper Age glacier mumm

207 n risk factor for gastric adenocarcinoma) on H. pylori diversification within a host.

208 also exerted a potent bactericidal effect on H. pylori as revealed by propidium iodide uptake and a m

209 nd harmful and we should therefore focus our H. pylori eradication policy toward selectively identify

210 Reanalysis of paired H. pylori genomes from chronically infected people demon

211 ter membrane protein diversity in persistent H. pylori infection.

212 These results indicate that persistent H. pylori infections acquired early in life are associat

213 In conclusion, CagA-positive H. pylori strains stimulate MMP10 expression.

214 d higher frequency of virulent cagA-positive H. pylori than those free of fluke infection.

215 CagA multimerization (CM) sequence-positive H. pylori.

216 ing mice, providing perspectives on possible H. pylori eradication therapies.

217 At 6 months postinoculation,H. pylori had successfully colonized within the gastric

218 didates are identified, all of which prevent H. pylori growth at concentrations 16-2000-fold lower th

219 c triple treatments for Helicobacter pylori (H. pylori) are increasingly unsuccessful.

220 herapy resistance, with Helicobacter pylori (H. pylori) infection being a major risk factor.

221 Helicobacter pylori (H. pylori) is a species of bacteria that can colonize th

222 Helicobacter pylori (H. pylori) is the strongest identified risk factor for g

223 that colonization with Helicobacter pylori (H. pylori) may affect body mass index (BMI), but with in

224 ported in patients with Helicobacter pylori (H. pylori)-infected gastric mucosa with intestinal metap

225 may be reused to detect Helicobacter pylori (H. pylori).

226 hic gastritis changes; 3) patients receiving H. pylori eradication triple therapy and 8 weeks of main

227 modH5 expression plays a role in regulating H. pylori motility phenotypes.

228 esence and abundance of antibiotic-resistant H. pylori strains, such processes are relatively expensi

229 osis of the presence of antibiotic-resistant H. pylori strains.

230 Second, H. pylori also induces VacA-independent alteration of mi

231 and ubiquitously present in all 69 sequenced H. pylori genomes at the same genomic locus, as well as

232 of the coastal town Tumaco, despite similar H. pylori prevalences.

233 Recently, some H. pylori strains were found to express resistance to a

234 However, successful H. pylori eradication is a more important factor for GU

235 4SS is required for TLR9 activation and that H. pylori DNA is actively translocated by the cag T4SS t

236 It is established that H. pylori stimulates neutrophil chemotaxis and a robust

237 In addition, we found that H. pylori might activate ATM through histone H3 and H4 h

238 We demonstrate here that H. pylori induces N1-like subtype differentiation of hum

239 These findings support the hypothesis that H. pylori contributes to the pathogenesis of chronic opi

240 In this study, we identified that H. pylori infection stimulated DNA damage, and therefore

241 These results also indicate that H. pylori has evolved to integrate expression of the maj

242 These data indicate that H. pylori infection can cause IDA and that the compositi

243 We propose that H. pylori has evolved a sensitive urea chemodetection an

244 t & Microbe, Huang et al. (2015) report that H. pylori employs its urease enzyme to destroy urea to b

245 The results show that H. pylori completely dominates the microbiota not only i

246 and infection of a mouse model, we show that H. pylori deregulates mitochondria by two novel mechanis

247 Our findings suggest that H. pylori coinfection effectuates a systemic immune modu

248 e from epidemiological studies suggests that H. pylori infection is associated with an estimated 18%

249 The H. pylori population inside the stomach contains a subgr

250 f the signature motifs in all arginases, the H. pylori homolog has a non-conserved motif ((153)ESEEKA

251 tion and oxidative stress and influenced the H. pylori transcriptome.

252 We isolated the H. pylori gene encoding this enzyme, bioV, by complement

253 ds zinc and represses the elaboration of the H. pylori cag type IV secretion system (T4SS).

254 ich reconciles the observed stability of the H. pylori gene content and its highly recombinational po

255 Furthermore, whole-cell studies on the H. pylori J99 reference strain confirmed the high effici

256 broth alone as an uninfected control or the H. pylori strain PMSS1.

257 Marygorret Obonyo, who provided the H. pylori SS1 strain for this work and participated in t

258 was examined by using RNA-seq to search the H. pylori transcriptome for RNAs whose 5'-phosphorylatio

259 We previously demonstrated that the H. pylori cag(+) strain 7.13 rapidly induces gastric can

260 tically, we show for the first time that the H. pylori cancer-associated cag T4SS is required for TLR

261 We report here that the H. pylori CheZ, CheZ(HP), localizes to the poles indepen

262 Here, we report that the H. pylori ImaA protein (HP0289) decreases the action of

263 Serologic testing for antibodies to H. pylori remains the most commonly ordered diagnostic t

264 ich BabA's adaptive evolution contributes to H. pylori persistence and overt gastric disease.

265 e TLR2/NLRP3/CASP1/IL-18 axis is critical to H. pylori-specific immune regulation.

266 We show that glutamate produced due to H. pylori gGT enzymatic activity tolerizes DCs by inhibi

267 t with the hypothesis that early exposure to H. pylori is inversely associated with atopy and allergi

268 ifferentiation were decreased in response to H. pylori.

269 ta) and inducible NO synthase in response to H. pylori.

270 in modulating host inflammatory responses to H. pylori, allowing the bacteria to persist and induce c

271 ed Th1 and Th17 adaptive immune responses to H. pylori, which contributed to decreased chronic inflam

272 ive percent of controls were seropositive to H. pylori.

273 order to still be able to effectively treat H. pylori infections in the future we need an alternativ

274 vivo therapeutic use of micromotors to treat H. pylori infection.

275 , and clarithromycin, commonly used to treat H. pylori infections.

276 Post-treatment H. pylori status was confirmed by a (13)C-urea breath te

277 evels of alpha5beta1 integrin than wild-type H. pylori, an outcome that required the predicted integr

278 ammation and cancer in response to wild-type H. pylori.

279 Using H. pylori arginase, our studies reveal that the interact

280 gene expression, and the mechanisms whereby H. pylori regulates NO synthesis by host cells.

281 provide a novel molecular mechanism by which H. pylori manipulates the host's immune response to pers

282 Our results thus suggest a model in which H. pylori employs ImaA to regulate interactions between

283 mice with H. pylori or treated animals with H. pylori components (bacterial lysate or the immunomodu

284 by H. pylori Infection of gastric cells with H. pylori led to an increase in levels of MMP-10 messeng

285 elonged to the European type consistant with H. pylori in Bhutan representing an intermediate evoluti

286 Serial infections of Mongolian gerbils with H. pylori strain 7.13 identified an oscillating pattern

287 ism associating ATM signaling induction with H. pylori infection.

288 KN45, and KATO III were either infected with H. pylori or left uninfected.

289 Mice that had been infected with H. pylori or treated with H. pylori-derived immunomodula

290 s biopsy samples from patients infected with H. pylori showed significant up-regulation of both Mcl1

291 intestinal metaplasia were all infected with H. pylori strains containing a specific cagA motif.

292 vious study demonstrated that infection with H. pylori HpslyD-positive strains associated with IM.

293 rexpression of miR-124 before infection with H. pylori prevented the induction of SMOX believed to co

294 estigate whether experimental infection with H. pylori, or prophylactic treatment with H. pylori-deri

295 HIF-1(Deltamyel) mice inoculated with H. pylori for 6 mo presented with a similar bacterial co

296 e infected neonatal C57BL/6 or C3H mice with H. pylori or treated animals with H. pylori components (

297 been infected with H. pylori or treated with H. pylori-derived immunomodulators showed reduced anaphy

298 Prophylactic treatment with H. pylori-derived immunomodulators appears to be a promi

299 th H. pylori, or prophylactic treatment with H. pylori-derived immunomodulatory molecules, affects th

300 esulted in M1 macrophage polarization within H. pylori-infected stomachs, as assessed by Luminex tech