ライフサイエンスコーパス: H. pylori

1 H. pylori bacterial load correlated positively with inte

2 H. pylori cagY sequence differences and cagT4SS function

3 H. pylori cell shape mutants show impaired colonization

4 H. pylori colonizes the human gastric mucosa and persist

5 H. pylori has an unusually large number of DNA methyltra

6 H. pylori infection has been associated with the introdu

7 H. pylori infection may have a pathophysiological role i

8 H. pylori infection of Nod1(-/-) mice led to significant

9 H. pylori infection rate were 90.26% in these cases, so

10 H. pylori proteins interfere with multiple host pathways

11 H. pylori resides in close proximity to S-phase cells in

12 H. pylori secretes a pore-forming toxin called vacuolati

13 H. pylori strains containing the cag pathogenicity islan

14 H. pylori virulence genes are highly prevalent and diver

15 H. pylori was identified in 368 samples, which were excl

16 H. pylori-induced nuclear factor kappa-light-chain-enhan

17 H. pylori-specific Ig are encoded by V and J family gene

18 In Cohort 1, H. pylori eradication was associated with a significant

19 fected adults, and analyze the genomes of 10 H. pylori isolates from each biopsy.

20 From January 2016 to January 2017, 133 H. pylori-infected gastric biopsy specimens were identif

21 biopsies from multiple stomach regions of 16 H. pylori-infected adults, and analyze the genomes of 10

22 ats per group): (1) control group (Con); (2) H. pylori infected group (HP): the rats were inoculated

23 ce analysis of the mod-4a/4b locus across 74 H. pylori strain genomes has provided insights into the

24 Gastric biopsies of 814 H. pylori infected patients naive for treatment were ana

25 ermine prevalence and determinants of active H. pylori infection in this population.

26 lter microbial phenotypes of in vivo-adapted H. pylori, we investigated host immunologic responses.

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

28 uestioned whether DFMO might directly affect H. pylori pathogenicity.

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

30 l NF-kappaB signaling was shown to aggravate H. pylori-induced gastric inflammation via activation of

31 Among H. pylori seropositive vaccine recipients, there were no

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

33 on to oral cholera vaccine CVD 103-HgR among H. pylori seropositive African adults provides further e

34 ody seroconversion was markedly higher among H. pylori seropositives than seronegatives 64% vs. 26% (

35 studies showed that there is variation among H. pylori strains in the steady-state levels of CagA and

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

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

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

39 uation of inflammatory cell infiltration and H. pylori colonization.

40 reductions of gastric spermidine levels and H. pylori-induced inflammation.

41 We included 22 mothers and H. pylori infection was determined by fecal antigen test

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

43 of infection by pathogenic bacteria, such as H. pylori, that exploit the epithelial mucosal surface t

44 hrough community engagement, community-based H. pylori screening and stomach cancer prevention is fea

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

46 We evaluated the association between H. pylori and the progression of colorectal adenoma.

47 N: In overall a positive association between H. pylori infection and diabetes mellitus was found.

48 rformed to determine the association between H. pylori infection and the risk of diabetes mellitus.

49 e pooled estimate of the association between H. pylori infection with diabetes was OR = 1.27 (95% CI

50 Associations between H. pylori gene polymorphisms and stomach niches suggest

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

52 How the interactions between H. pylori and its host shape the gastric environment dur

53 results uncovered a mechanistic link between H. pylori infection and miR-135b-5p-KLF4, suggesting tha

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

55 ults about the possible relationship between H. pylori and diabetes.

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

57 udies investigating the relationship between H. pylori infection and diabetes mellitus.

58 dulation of epithelial-derived chemokines by H. pylori infection will be discussed.

59 ell morphology promotes host colonization by H. pylori, we used three-dimensional confocal microscopy

60 The strong inflammatory response elicited by H. pylori is characterized by the induction of the expre

61 mitochondrial localization of LC3 induced by H. pylori infection were attenuated in AGS cells harbori

62 vent or treat pathologic outcomes induced by H. pylori infection.

63 Inhibition of Siva1 by H. pylori increases survival of human cells with damaged

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

65 fected or subsequently infected with cag (+) H. pylori or an isogenic cagE (-) mutant (nonfunctional

66 noninvasive assessment of the ulcer-causing H. pylori gastric pathogen.

67 In conclusion, chronic H. pylori infection stimulates Lrig1-expressing progenit

68 y represent a therapeutic target for chronic H. pylori infection.

69 overexpression of Rspo3 in the stroma clears H. pylori from the gastric glands.

70 aim of this study was to identify the common H. pylori virulence genes among dyspeptic Southwestern S

71 h wild type mice, Nlrc4(-/-) mice controlled H. pylori better without showing strong inflammation.

72 imary study event, 25% of whom had a current H. pylori infection.

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

74 ty as measured by participation in a one-day H. pylori screening initiative, and participation in fol

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

76 For laboratory studies, well-defined H. pylori strain B128 and its cancerogenic derivative st

77 In detail, we can detect H. pylori both on Giemsa- and regular H&E stained whole

78 -generation sequencing (NGS) assay to detect H. pylori mutations that are known to confer resistance

79 The method successfully detected H. pylori in 126 of 133 cases (95% sensitivity).

80 ally aid pathologists to accurately diagnose H. pylori presence on gastric biopsies.

81 independently introduced into two different H. pylori types, termed pre-type-A and pre-type-B, which

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

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

84 s like ammonia, potentially generated during H. pylori infection by urease and other enzymes, enhance

85 ed the role of the NLRC4 inflammasome during H. pylori infection.

86 tudy, we conducted a pilot community-engaged H. pylori education and screening study in partnership w

87 studied the association between pre-existing H. pylori serum IgG and serum pepsinogens levels (PGs) a

88 Helical cell shape is thought to facilitate H. pylori's ability to bore into the protective mucus la

89 All 22 infants tested negative for fecal H. pylori at 15 days of age, but those born vaginally -a

90 cted with a mixture of isogenic, fluorescent H. pylori strains with unprecedented spatial resolution.

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

92 ion systems, was shown to be dispensable for H. pylori-induced inflammasome activation.

93 to investigate the components necessary for H. pylori chemotaxis.

94 eriological testing of subjects negative for H. pylori becomes clinically relevant and important.

95 ithelial cells has implications not only for H. pylori pathogenesis but for host tumorigenesis.

96 proving as a sensitive screening option for H. pylori that can potentially aid pathologists to accur

97 rs, we found that only TlpB was required for H. pylori accumulation, while TlpA, TlpC, and TlpD were

98 Cagalpha and CagE were required for H. pylori-induced NF-kappaB activation, IL-8 secretion,

99 thways to generate a protected reservoir for H. pylori that confers bacterial survival in vitro.

100 ase specificity) as a valuable substrate for H. pylori HtrA.

101 ong 93 healthy Malian adults were tested for H. pylori IgG antibodies and PGI and PGII levels using e

102 sy specimen from each subject was tested for H. pylori.

103 ients, who did not receive any treatment for H. pylori.

104 ic decisions, where antibiotics are used for H. pylori eradication.

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

106 cells, we quantified cytokine secretion from H. pylori-infected primary gastric organoids generated f

107 Furthermore, H. pylori infection altered the polarization status of N

108 Furthermore, H. pylori-infected Neil2-KO mice had greater inflammatio

109 ithout gastritis, oral H. pylori and gastric H. pylori in the percentage of sites with gingival bleed

110 Of these, 34.2% had gastric H. pylori and 5% had oral H. pylori.

111 assess gastritis and the presence of gastric H. pylori using Giemsa stain.

112 r gastritis, the presence of oral or gastric H. pylori.

113 In this study, we generated H. pylori strains producing chimeric proteins in which V

114 Here, we present a new model of how H. pylori establish and persist in stomach, which involv

115 To get a more complete picture of how H. pylori regulates the T4SS during animal colonization,

116 ronic H. felis infection, which mimics human H. pylori infection in mice, we reveal a key role for pS

117 Importantly, H. pylori-induced replication stress and DNA damage depe

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

119 ss DNA damage and beta-catenin activation in H. pylori-infected Smox(-/-) mice or gastric organoids,

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

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

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

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

124 as an independent predictive marker of GC in H. pylori-infected but not -eradicated patients.

125 in non-IM may be a surrogate marker of GC in H. pylori-infected patients.

126 e demonstrated the essential role of HtrA in H. pylori physiology and pathogenesis.

127 3 other essential cagPAI genes implicated in H. pylori T4SS function, most commonly cag5, cag10, and

128 dormant bacteria that might be important in H. pylori infections refractory to treatment.

129 ncodes for a truncated and inactive MTase in H. pylori strain 26695.

130 Beyond this, the role of NOD1 in H. pylori-induced cancer remains undefined.

131 of antral mucosal iNOS(+) and iNOS(-) PC in H. pylori infection, we sequenced rearranged Ig genes fr

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

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

134 conclusion, DFMO-induced oxidative stress in H. pylori leads to genomic alterations and attenuates vi

135 e show that expression of the AapA1 toxin in H. pylori causes growth arrest associated with rapid mor

136 forming DNA during natural transformation in H. pylori.

137 f gastric infections while the variations in H. pylori detection and the associated risk factors inve

138 T3 is a feature of gastric cancer, including H. pylori-infected tissues, and aligns with nuclear tran

139 t with protection from chronic inflammation, H. pylori-infected IL-21(-/-) mice exhibited limited Th1

140 8 (IL-8) value of <0.3 relative to the input H. pylori strain PMSS1.

141 The participants were divided into H. pylori-infected and NHPGH-infected groups, based on t

142 e models to provide mechanistic insight into H. pylori's ability to delay apoptosis in gastric epithe

143 ted the impact of the apparent intracellular H. pylori (aiHp) on treatment failure of first-line trip

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

145 es a bone marrow-derived macrophage and live H. pylori co-culture with global time-course transcripto

146 N in its unusual menaquinone pathway, making H. pylori MTAN a target for antibiotic development.

147 erences in the infant microbiota by maternal H. pylori status (PERMANOVA, p = 0.01), with higher abun

148 We hypothesized that maternal H. pylori status affects the maternal intestinal microbi

149 fecal microbiota is affected by the maternal H. pylori status only in infants born vaginally, suggest

150 rs and their babies differed by the maternal H. pylori status, only in vaginal birth, not in C-sectio

151 n mothers and neonates according to maternal H. pylori status and delivery mode.

152 ing from gastritis and nonexistence of mixed H. pylori infection, bacteriological testing of subjects

153 Moreover, H. pylori-induced IL-18 inhibits beta-defensin 1 express

154 ine gastric organoids (gastroids) and mutant H. pylori strains to investigate the components necessar

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

156 Finally, a total of 60 non-H. pylori samples were studied for NHPGH species.

157 Notably, H. pylori-infected AGS cells exhibited the loss of mitoc

158 roid lumen, it prevented the accumulation of H. pylori at damage sites.

159 In summary, WGS allows for broad analyses of H. pylori isolates, and our findings support the use of

160 the association between oral colonization of H. pylori and dental diseases.

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

162 Routine detection of H. pylori mutations that invoke antimicrobial resistance

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

164 Development of H. pylori-associated diseases is determined by a number

165 The effect of H. pylori infection on diabetes mellitus (both types), t

166 ed in Asian population risk of the effect of H. pylori infection on diabetes was slightly higher than

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

168 We evaluated the effects of H. pylori eradication (Cohort 1) and aspirin use (Cohort

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

170 lopment and, after successful eradication of H. pylori, the colorectal adenoma ratio might decrease.

171 CLA resistance is associated with failure of H. pylori eradication.

172 ite high infection rates, only a fraction of H. pylori-infected individuals develop gastric cancer.

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

174 r evidence of the immunomodulating impact of H. pylori on oral vaccine immunogenicity.

175 fied Zn(++) and Cu(++) ions as inhibitors of H. pylori HtrA activity, as monitored by in vitro cleava

176 tion in either non-IM or IM, irrespective of H. pylori infection.

177 E enzyme and the Cag pathogenicity island of H. pylori, is accompanied by replication fork stalling a

178 HGT from an antibiotic-resistant isolate of H. pylori We find that HGT increases the rate of adaptat

179 m facilitated complement-mediated killing of H. pylori and E. cloacae, indicating its potential as a

180 lation were increased in the mitochondria of H. pylori-inoculated mouse stomach.

181 s of function studies with in vivo models of H. pylori infection as well as a chemically-induced mode

182 The highest number of H. pylori isolates 76.9% (180/234) was obtained from pat

183 mucosa contribute to spatial partitioning of H. pylori populations.

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

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

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

187 ed the expression of CD40 in the presence of H. pylori Also, Th17 recall responses were intact when D

188 The global prevalence of H. pylori approaches 50%, with prevalence rates between

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

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

191 study aimed at determining the prevalence of H. pylori infections and virulence genes (cagA, dupA, an

192 Prevalence of H. pylori, and, correspondingly, stomach cancer incidenc

193 ional to accelerate the detection process of H. pylori on histological specimens, using novel technol

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

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

196 role in shaping the population structure of H. pylori.

197 cell polarity and decreases the survival of H. pylori in infected organoids.

198 y, we demonstrate that in vitro treatment of H. pylori by DFMO induces oxidative DNA damage, expressi

199 e the effect of clarithromycin resistance on H. pylori eradication in a population from Santiago, and

200 (1) the association between gastric and oral H. pylori colonization and (2) the association between o

201 this study, the presence of gastric and oral H. pylori in patients with good oral hygiene and moderat

202 polymerase chain reaction PCR to detect oral H. pylori.

203 en patients with and without gastritis, oral H. pylori and gastric H. pylori in the percentage of sit

204 34.2% had gastric H. pylori and 5% had oral H. pylori.

205 Of the 444 participants, H. pylori was detected in 115 (25.9%) from culture analy

206 Persistent H. pylori infection was associated significantly with th

207 hes in the gastric glands house a persistent H. pylori reservoir, which we propose replenishes the mo

208 progression in participants with persistent H. pylori infections (persistent group) and those whose

209 Blockade of cagA-positive H. pylori ASPP2 signaling by inhibitors of the EGFR (epi

210 contributes to the survival of cagA-positive H. pylori in the lumen of infected gastric organoids.

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

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

213 The most potent H. pylori virulence factor is cytotoxin-associated gene

214 ention forward to population-based precision H. pylori screening and eradication.

215 In summary, mucosal iNOS(+) PC producing H. pylori-specific Ig accumulate in infection and appear

216 These findings indicate that SMOX promotes H. pylori-induced carcinogenesis by causing inflammation

217 the association between Helicobacter pylori (H. pylori) and dental diseases with possible effect of e

218 cer (GC) declines after Helicobacter pylori (H. pylori) eradication and long-term aspirin use.

219 Helicobacter pylori (H. pylori) eradication using standard triple therapy (ST

220 Helicobacter pylori (H. pylori) infection is a major cause of chronic gastrit

221 Helicobacter pylori (H. pylori) infection is considered as one of the princip

222 triggered by persistent Helicobacter pylori (H. pylori) infection.

223 Helicobacter pylori (H. pylori) is the strongest known risk for gastric cance

224 Helicobacter pylori (H. pylori) secretes the chaperone and serine protease hi

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

226 the enzyme ornithine decarboxylase, reduces H. pylori-mediated gastric cancer incidence in Mongolian

227 Treatment of AGS cells with OM-NPs reduces H. pylori adhesion and such anti-adhesion efficacy is de

228 pothesize that IL-21 may indirectly regulate H. pylori-specific T cell responses by controlling dendr

229 Remarkably, H. pylori that lack toxigenic VacA colonize enlarged dys

230 han those present in straight- or curved-rod H. pylori.

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

232 fector of coccoids to be identified, targets H. pylori inner membrane without disrupting it, as visua

233 s significantly higher levels of IL-17A than H. pylori-infected wild-type (WT) mice in the Peyer's pa

234 Overall, our findings demonstrate that H. pylori colonizes and limits repair at damage sites vi

235 We found that H. pylori compromises key tumor suppressor mechanisms: t

236 g the infected stomach lining, we found that H. pylori infection is associated with the production of

237 We found that H. pylori is resistant to killing by millimolar concentr

238 These results indicate that H. pylori eradication and aspirin use were less effectiv

239 Here we report that H. pylori-infected IL-21(-/-) mice express significantly

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

241 ers from healthy human stomach, we show that H. pylori infection greatly reduces NEIL2 expression.

242 We show that H. pylori output strains isolated from gerbils treated w

243 Here, we show that H. pylori-induced DNA damage occurs co-transcriptionally

244 ites of tissue inflammation, a strategy that H. pylori uses to aid in colonizing and persisting in in

245 We demonstrated previously in vivo that H. pylori uses motility to preferentially colonize injur

246 The H. pylori Cag T4SS includes a large membrane-spanning co

247 The H. pylori cag type IV secretion system is an oncogenic l

248 The H. pylori eradication rate was 63% and the prevalence of

249 The H. pylori infection-induced downregulation of NEIL2 was

250 ter understand the role of M.HpyAXVII in the H. pylori biology, here we cloned and overexpressed the

251 Notably, the H. pylori-infected Neil2-KO murine stomach exhibited mor

252 The molecular architecture of the H. pylori Cag T4SS is substantially more complex than th

253 These results reveal that assembly of the H. pylori T4SS core complex is dependent on incorporatio

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

255 o genetic models of Nod1 deficiency with the H. pylori cag (+) strain PMSS1: C57BL/6 mice, which rare

256 Nickel binding to H. pylori NikR (HpNikR) induces an allosteric response f

257 cteriaceae and Veillonella, in those born to H. pylori-positive mothers.

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

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

260 Two clones reacted to H. pylori proteins, and five were found to be polyreacti

261 IL-26) in regulating the immune response to H. pylori colonization and carcinogenesis.

262 ; however, their contribution in response to H. pylori infection has not been fully elucidated.

263 uce proinflammatory cytokines in response to H. pylori While H. pylori increased the expression of co

264 mines are regulators of the host response to H. pylori, and that spermine oxidase (SMOX), which metab

265 ugments inflammatory and injury responses to H. pylori.

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

267 Wild-type H. pylori accumulated at the damage site after gastric d

268 cal centerline pitch and radius of wild-type H. pylori cells dictate surface curvatures of considerab

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

270 -) mice failed to produce gastric IL-18 upon H. pylori infection.

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

272 Using H. pylori isolates from 42 clinical specimens, we compar

273 Eleven mothers (50%) were H. pylori-positive (7 delivering vaginally and 4 by C-se

274 Overall 74/93 (80%) vaccine recipients were H. pylori IgG seropositive at baseline.

275 nation is the most common mechanism by which H. pylori downregulates T4SS function during murine infe

276 masse, elucidation of the mechanism by which H. pylori evolved to carry multiple copies of cagA helps

277 regulation is a plausible mechanism by which H. pylori infection impairs DNA damage repair, amplifies

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

279 idized bases, is one mechanism through which H. pylori infection may fuel the accumulation of DNA dam

280 While H. pylori is known to evolve during infection, populatio

281 ory cytokines in response to H. pylori While H. pylori increased the expression of costimulatory prot

282 ill advance our understanding of how and why H. pylori infection may be tolerated in some individuals

283 hypercolonization of the gastric glands with H. pylori, including the stem cell compartment.

284 rom human subjects and animals infected with H. pylori bacteria harboring different CagA status.

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

286 n gastric epithelial AGS cells infected with H. pylori resulted in localization of STAT3 phosphorylat

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

288 Infection with H. pylori induced the expression of miR-135b-5p in the i

289 Infection with H. pylori is the main risk factor for distal gastric can

290 ed group (HP): the rats were inoculated with H. pylori (10(8-) 10(10) CFU/mL; 1 mL/rat.) for 3 consec

291 up (HP + Gen): the rats were inoculated with H. pylori as above.

292 elium and the epithelium's interactions with H. pylori The focal point of this Brief Review will be o

293 of genistein and its mechanisms in rats with H. pylori infection.

294 n and gastric mucosal apoptosis in rats with H. pylori-induced gastropathy.

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

296 al adenoma ratio of patients uninfected with H. pylori was similar to that of the eradication group (

297 lls ex vivo and via lineage expansion within H. pylori-infected gastric mucosa.

298 WT H. pylori-infected mice harbored significantly higher nu

299 metaplasia marker) were increased only by WT H. pylori In human samples, Lrig1 expression was signifi

300 In contrast to infection with wild-type (WT) H. pylori for 2 wk, infection for 8 wk resulted in signi