ライフサイエンスコーパス: Helicobacter

1 ssified Comamonadaceae, Cloacibacterium, and Helicobacter.

2 ease in the abundance of the bacterial genus Helicobacter.

3 RISPR-Cas9 gene editing) were incubated with Helicobacter and gene expression and production of cytok

4 sociations among infection with liver fluke, Helicobacter and hepatobiliary fibrosis.

5 sthorchis viverrini serves as a reservoir of Helicobacter and implicate Helicobacter in pathogenesis

6 was enriched in oxygen-tolerant taxa (e.g., Helicobacter and Treponema), while the lumenal microbiot

7 effects on ILCs by two Helicobacter species, Helicobacter apodemus and Helicobacter typhlonius, isola

8 nome sequences where Alphapapillomavirus and Helicobacter are detected in addition to a variety of ot

9 In this model system, the pathobiont Helicobacter bilis instigates disease following sub-path

10 pes from multiple human pathogens, including Helicobacter, Chlamydia, Brucella, and Campylobacter.

11 ion to active tuberculosis is altered by gut Helicobacter co-infection, (2) aerosol Mycobacterium tub

12 pS-STAT3 dependency by Helicobacter coincided with transcriptional activity on

13 ial as a supportive therapy during and after Helicobacter eradication therapy.

14 pe (WT) and APRIL Tg mice were infected with Helicobacter felis and Helicobacter pylori and compared

15 Some mice were gavaged with H pylori SS1 or Helicobacter felis; 3 months later, stomachs, spleens, a

16 ight for the first time that arginase of all Helicobacter gastric pathogens utilizes a unique non-cat

17 wo residues exclusively in arginase of other Helicobacter gastric pathogens, which may have similar f

18 th critical residues in the homolog of other Helicobacter gastric pathogens.

19 Helicobacter (H.) pylori is primarily an extracellularly

20 Helicobacter (H.) suis causes gastric pathologies in bot

21 In the absence of IL-10, Helicobacter hepaticus (Hh) induces colitis.

22 Helicobacter hepaticus is a member of the mouse intestin

23 is an emerging human foodborne pathogen, and Helicobacter hepaticus is a mouse pathogen; both species

24 c, pathology in C57BL/6 mice inoculated with Helicobacter hepaticus plus anti-IL-10 receptor (IL-10R)

25 In this study, we show using Helicobacter hepaticus-induced intestinal inflammation t

26 We show that Helicobacter htrA is an essential bifunctional gene with

27 as a reservoir of Helicobacter and implicate Helicobacter in pathogenesis of opisthorchiasis-associat

28 IL-11 signaling via constitutive pS-STAT3 in Helicobacter-induced gastric carcinogenesis.

29 reveal a key role for pS-STAT3 in promoting Helicobacter-induced gastric pathology.

30 Lineage tracing in Helicobacter-infected Slfn4 reporter mice revealed that

31 on may help reducing tissue damage caused by Helicobacter infection in both humans and pigs, highligh

32 romote B-cell lymphomagenesis during chronic Helicobacter infection.

33 taining 5 (NLRC5), in patients and mice with Helicobacter infection.

34 was constitutively expressed irrespective of Helicobacter infection.

35 nd mucosal lymphoid formation in response to Helicobacter infection.

36 r development of drugs to specifically treat Helicobacter infections.

37 A hypothesis that a "Helicobacter-like" process causes PC justified this pilo

38 bundance of Campylobacter and a reduction in Helicobacter macacae.

39 rium damsela alpha2-6-sialyltransferase, and Helicobacter mustelae alpha1-2-fucosyltransferase, as ef

40 Two Helicobacter mutant strains (katA(H56A) and katA(Y339A))

41 Non Helicobacter pylori gastric Helicobacters (NHPGHs) are associated with a range of up

42 oborated using two different PGTs; PglC from Helicobacter pullorum and WecA from Thermatoga maritima.

43 Helicobacter pullorum is an emerging human foodborne pat

44 In patients with chronic Helicobacter pylori (H pylori) infection, parietal and c

45 stent evidence about the association between Helicobacter pylori (H. pylori) and dental diseases with

46 Empiric triple treatments for Helicobacter pylori (H. pylori) are increasingly unsucce

47 e risk of gastric cancer (GC) declines after Helicobacter pylori (H. pylori) eradication and long-ter

48 Helicobacter pylori (H. pylori) eradication using standa

49 er mortality due to therapy resistance, with Helicobacter pylori (H. pylori) infection being a major

50 Helicobacter pylori (H. pylori) infection is a major cau

51 Helicobacter pylori (H. pylori) infection is considered

52 ammation (gastritis) triggered by persistent Helicobacter pylori (H. pylori) infection.

53 Helicobacter pylori (H. pylori) is a species of bacteria

54 Helicobacter pylori (H. pylori) is the strongest identif

55 Helicobacter pylori (H. pylori) is the strongest known r

56 cal studies indicated that colonization with Helicobacter pylori (H. pylori) may affect body mass ind

57 Helicobacter pylori (H. pylori) secretes the chaperone a

58 -proliferation was reported in patients with Helicobacter pylori (H. pylori)-infected gastric mucosa

59 ve rapid urease test may be reused to detect Helicobacter pylori (H. pylori).

60 Helicobacter pylori (H.pylori) infections are prevalent

61 f of the world's population is infected with Helicobacter pylori (H.pylori), a bacterium shown to be

62 Co-infection between Helicobacter pylori (Hp) and groups of periodontal patho

63 Helicobacter pylori (HP) colonizes the human stomach and

64 long-term complete remission after frontline Helicobacter pylori (HP) eradication (HPE).

65 We evaluated the effect of Helicobacter pylori (HP) eradication on p53, cyclin D1 e

66 Helicobacter pylori (HP) infection is present in about 5

67 Helicobacter pylori (Hp) infection is the main cause of

68 It is known that the prevalence of Helicobacter pylori (Hp) infection, a risk factor for ga

69 Helicobacter pylori (Hp) secrete VacA, a diffusible pore

70 Helicobacter pylori (Hp) strains that carry the cag type

71 bination of serum pepsinogens(PGs), IgG anti-Helicobacter pylori (HpAb), and osteopontin (OPN) can be

72 alpha-Carbonic anhydrase of Helicobacter pylori (HpalphaCA) plays an important role

73 acterized the binding of parS and Spo0J from Helicobacter pylori (HpSpo0J) and solved the crystal str

74 mologs from Campylobacter coli (R.CcoLI) and Helicobacter pylori (R.HpyAXII) and demonstrated their D

75 The Helicobacter pylori adhesin BabA binds mucosal ABO/Le(b)

76 l. (2016) perform structural analyses of the Helicobacter pylori adhesin BabA to determine how the ba

77 Combining these enzymes with Helicobacter pylori alpha1-3-fucosyltransferase, we deve

78 Several important human pathogens, such as Helicobacter pylori and Campylobacter jejuni, have escap

79 ator of M1 macrophage activation during both Helicobacter pylori and Citrobacter rodentium infection.

80 ce were infected with Helicobacter felis and Helicobacter pylori and compared with noninfected animal

81 Pse on their surface polysaccharides (e.g., Helicobacter pylori and Enterobacter cloacae), revealing

82 One example is Helicobacter pylori and gastric cancer.

83 Clinically, Helicobacter pylori and GC-associated UHMK1 mutation ind

84 pathogens is being recognized, for example, Helicobacter pylori and human papillomavirus in the case

85 oid cells also reduced the T(H)1 response to Helicobacter pylori and impaired immune control of the b

86 Colonization of the human stomach by Helicobacter pylori and its role in causing gastric canc

87 study, OM-NPs are made with the membrane of Helicobacter pylori and shown to bind with gastric epith

88 Although Helicobacter pylori and use of non-steroidal anti-inflam

89 Helicobacter pylori antibiotic resistance is widespread

90 enocarcinoma and seropositivity to different Helicobacter pylori antigens using multiplex serology ha

91 Helicobacter pylori arginase, a bimetallic enzyme, is cr

92 of cancer death worldwide, is infection with Helicobacter pylori bacterial strains that inject cytoto

93 Expression of the Helicobacter pylori blood group antigen binding adhesin

94 The Helicobacter pylori Cag T4SS translocates CagA, a bacter

95 Heterogeneity at the Helicobacter pylori cagA gene promoter region has been l

96 Helicobacter pylori CagA is a secreted effector protein

97 ation of particular polymorphisms within the Helicobacter pylori CagL hypervariable motif (CagLHM) in

98 ave recently found that the gastric pathogen Helicobacter pylori can activate gastric stem cells and

99 Lifelong infection of the gastric mucosa by Helicobacter pylori can lead to peptic ulcers and gastri

100 : Despite inducing an inflammatory response, Helicobacter pylori can persist in the gastric mucosa fo

101 tly associated with sex, breast-feeding, and Helicobacter pylori carriership.

102 We report on the protonation state of Helicobacter pylori catalase compound II.

103 epithelial cells to the bacterial carcinogen Helicobacter pylori causes DNA double strand breaks.

104 ution crystal structure of dCACHE LBD of the Helicobacter pylori chemoreceptor TlpC.

105 Chronic Helicobacter pylori colonization in animal models often

106 Helicobacter pylori colonization may affect the mucosal

107 Helicobacter pylori colonizes the gastric mucosa and sec

108 Helicobacter pylori colonizes the human stomach and cont

109 Helicobacter pylori colonizes the human stomach and incr

110 Helicobacter pylori colonizes the stomach in about half

111 Helicobacter pylori colonizes the stomach of around 50%

112 Helicobacter pylori confers protection against the anaph

113 We surveyed national Helicobacter pylori diagnostic testing practices and dia

114 Helicobacter pylori differentially binds SPEM glands in

115 The human pathogen Helicobacter pylori displays extensive genetic diversity

116 We found that Helicobacter pylori DNA can be detected in human stool s

117 The Helicobacter pylori energy sensor TlpD determines tactic

118 Helicobacter pylori eradication and endoscopic surveilla

119 Helicobacter pylori eradication rates in Portugal are de

120 Helicobacter pylori eradication therapy to prevent gastr

121 Rifabutin-based triple therapy (RHB-105) for Helicobacter pylori eradication: a double-blind, randomi

122 hich is solely a GTPase, the V. cholerae and Helicobacter pylori FeoB proteins have both GTPase and A

123 s lumazine synthase (LuS) and the 24-subunit Helicobacter pylori ferritin.

124 Interestingly, Helicobacter pylori flagellin triggered robust Nlrc4 pho

125 s homologs from Agrobacterium, Brucella, and Helicobacter pylori form heterodimers.

126 he gastric tissues of patients infected with Helicobacter pylori from gastritis to precancerous intes

127 Non Helicobacter pylori gastric Helicobacters (NHPGHs) are a

128 umulating evidence indicates that persistent Helicobacter pylori gastric infection influences immune

129 antified the expression of a large number of Helicobacter pylori genes and found high expression of g

130 Helicobacter pylori genetic diversity is known to be inf

131 Helicobacter pylori GroES (HpGroES), a potent immunogen,

132 helical shape of the human stomach pathogen Helicobacter pylori has been suggested to provide mechan

133 The emergence of drug resistance in Helicobacter pylori has resulted in a greater need for s

134 -sensitive populations of the human pathogen Helicobacter pylori in an environment without antibiotic

135 We detected Helicobacter pylori in only the upper GI tract.

136 evalence of primary antibiotic resistance in Helicobacter pylori in the Asia-Pacific region.

137 for the survival of the pathogenic bacteria Helicobacter pylori in the fluctuating pH of the human s

138 ions, particularly infections resulting from Helicobacter pylori in the gastric tract.

139 Half of all humans harbor Helicobacter pylori in their stomachs.

140 the Gram-negative, microaerophilic bacterium Helicobacter pylori induces an inflammatory response and

141 Helicobacter pylori induces strong inflammatory response

142 Helicobacter pylori induces the antiapoptotic protein my

143 A total of 200 Helicobacter pylori infected patients were retrospective

144 ive protein (aOR: 0.82; 95% CI: 0.73, 0.92), Helicobacter pylori infection (aOR: 0.11; 95% CI: 0.05,

145 wheat allergy (WA), coeliac disease (CD) and Helicobacter pylori infection (HP).

146 icting data regarding an association between Helicobacter pylori infection and iron deficiency anemia

147 Both the prevalence of Helicobacter pylori infection and the incidence of gastr

148 ing clarithromycin as a model antibiotic and Helicobacter pylori infection as a model disease.

149 Using Helicobacter pylori infection as a model for chronic muc

150 cing identified more IM patients with active Helicobacter pylori infection compared with histopatholo

151 ence from developed countries indicates that Helicobacter pylori infection correlates with a reduced

152 Eradication of Helicobacter pylori infection has been reported to reduc

153 The role of Helicobacter pylori infection in activating or favouring

154 Gastric injury, such as from Helicobacter pylori infection in patients with chronic a

155 Helicobacter pylori infection induces a number of pro-in

156 Helicobacter pylori infection is a major risk factor for

157 Helicobacter pylori infection is a proven carcinogen for

158 Helicobacter pylori infection is associated with colorec

159 Helicobacter pylori infection is characterized by chroni

160 Among other risk factors, Helicobacter pylori infection is considered the main dri

161 Helicobacter pylori infection is implicated in the aetio

162 Helicobacter pylori infection is increasingly difficult

163 Helicobacter pylori infection is the main risk factor fo

164 Helicobacter pylori infection is the main risk factor fo

165 Helicobacter pylori infection is the most important risk

166 Chronic Helicobacter pylori infection triggers neoplastic transf

167 amed stomachs (from TxA23 mice and mice with Helicobacter pylori infection) identified more metaplast

168 Risk factors for the condition include Helicobacter pylori infection, age, high salt intake, an

169 egulation of iNOS has been observed in human Helicobacter pylori infection, but the cellular sources

170 In human Helicobacter pylori infection, mucosal PC express induci

171 ncer databases, which do not include data on Helicobacter pylori infection, the most well-known risk

172 tric submucosal vessels in a murine model of Helicobacter pylori infection.

173 Chronic gastritis was induced in B6 mice by Helicobacter pylori infection.

174 ct the gastric epithelium, especially during Helicobacter pylori infection.

175 f non-steroidal anti-inflammatory drugs, and Helicobacter pylori infection.

176 ctiveness of standard therapies to eradicate Helicobacter pylori infection.

177 Although consensus supports eradication of Helicobacter pylori infections, antimicrobial resistance

178 Helicobacter pylori infects the human stomach and causes

179 Helicobacter pylori inhabits the gastric mucosa where it

180 Helicobacter pylori is a bacterial pathogen associated w

181 Helicobacter pylori is a Gram-negative bacterium that in

182 Helicobacter pylori is a gram-negative bacterium that pe

183 Helicobacter pylori is a human-specific pathogen that ch

184 Helicobacter pylori is a pathogen that chronically colon

185 Helicobacter pylori is a successful pathogen of the huma

186 Helicobacter pylori is accounted as the most etiologic a

187 Infection with Helicobacter pylori is associated with severe digestive

188 The bacterium Helicobacter pylori is one of the most common infectious

189 The stomach bacterium Helicobacter pylori is one of the most prevalent human p

190 BACKGROUND & AIMS: Helicobacter pylori is remarkable for its genetic variat

191 Infection by Helicobacter pylori is the primary cause of gastric aden

192 The bacteria Helicobacter pylori is the single leading carcinogenic i

193 Helicobacter pylori is the strongest risk factor for gas

194 Helicobacter pylori is the strongest risk factor for gas

195 distribution of shared gene pools for global Helicobacter pylori isolates.

196 Helicobacter pylori lacks a gene encoding a homologue of

197 tructure of a soluble variant of full-length Helicobacter pylori MotB in which the plug helix was eng

198 In a Helicobacter pylori mouse infection model, PMN infiltrat

199 The Helicobacter pylori MTAN (HpMTAN) hydrolyzes 6-amino-6-d

200 Hypergastrinemia occurred more frequently in Helicobacter pylori negative patients and of these 20/22

201 The Helicobacter pylori phase variable gene modH, typified b

202 The bacterium Helicobacter pylori possess only one OASS (hp0107) gene

203 Infection with the Gram-negative bacterium Helicobacter pylori remains the most important modifiabl

204 The gastric microbe Helicobacter pylori represents an ancestral constituent

205 The gastric pathogen Helicobacter pylori requires a noncanonical cytosolic ch

206 Helicobacter pylori secretes a pore-forming VacA toxin t

207 Helicobacter pylori specifically colonizes the human gas

208 Infection of the stomach with Helicobacter pylori stimulates increased secretion of Rs

209 Colonization of the human stomach with Helicobacter pylori strains containing the cag pathogeni

210 Most Helicobacter pylori strains express the BabA adhesin, wh

211 Infection with CagA+ Helicobacter pylori strains is linked to an increased ri

212 and gastric cancer are caused most often by Helicobacter pylori strains that harbor the cag pathogen

213 Helicobacter pylori strains that harbor the oncoprotein

214 erated against the O chain polysaccharide of Helicobacter pylori that contains polymeric Le(x) struct

215 bA adhesin mediates high-affinity binding of Helicobacter pylori to the ABO blood group antigen-glyco

216 Adherence of Helicobacter pylori to the gastric epithelial cell line

217 Adherence of Helicobacter pylori to the gastric epithelial cell line

218 Family history of gastric cancer and Helicobacter pylori treatment.

219 Helicobacter pylori type IV secretion system injects the

220 The gastric pathogen Helicobacter pylori undergoes host-mediated oxidant stre

221 as inhibitors of Sporosarcina pasteurii and Helicobacter pylori ureases.

222 Helicobacter pylori uses MTAN in its unusual menaquinone

223 The human pathogen Helicobacter pylori uses the host receptor alpha5beta1 i

224 Helicobacter pylori VacA is a secreted pore-forming toxi

225 of galectin-3 (Gal3) in gastric infection by Helicobacter pylori We first demonstrated that Gal3 was

226 In the gastric pathogen Helicobacter pylori we identify six distinct subtypes, o

227 ed from the chromosome of the human pathogen Helicobacter pylori We show that expression of the AapA1

228 s at the interface of the bacterial pathogen Helicobacter pylori with its host.

229 we present two high-resolution structures of Helicobacter pylori XerH with its recombination site DNA

230 ecific distribution of risk factors (such as Helicobacter pylori) can vary by race and ethnicity and

231 Helicobacter pylori, a 2 x 1 mum spiral-shaped bacterium

232 rophage EGFR signaling during infection with Helicobacter pylori, a bacterial pathogen that causes pe

233 The genome of the gastric pathogen Helicobacter pylori, a Gram-negative epsilonproteobacter

234 on Caulobacter crescentus, Vibrio cholerae, Helicobacter pylori, and Campylobacter jejuni, organisms

235 cquired infections, clarithromycin-resistant Helicobacter pylori, and fluoroquinolone-resistant Campy

236 entury, and shortly thereafter the bacterium Helicobacter pylori, and later Fusobacterium nucleatum,

237 forces do, however, appear to play a role in Helicobacter pylori, and some individual genes in all gr

238 g a highly prevalent gram-negative pathogen, Helicobacter pylori, as a model organism.

239 ce of this coincides with the eradication of Helicobacter pylori, both of which might alter the oesop

240 e in the evolution of the bacterial pathogen Helicobacter pylori, but its dynamics remain incompletel

241 tantly related species Bacillus subtilis and Helicobacter pylori, but its role in bacterial chemotaxi

242 essary for efficient stomach colonization by Helicobacter pylori, but the molecular mechanisms for ge

243 , in some cases such as the gastric pathogen Helicobacter pylori, HtrA is secreted where it cleaves t

244 isseria meningitidis, Neisseria gonorrhoeae, Helicobacter pylori, Moraxella catarrhalis, and Streptoc

245 results in more efficient immune control of Helicobacter pylori, Mycobacterium bovis bacillus Calmet

246 e human gastrointestinal microbiota, such as Helicobacter pylori, other members of the neonatal intes

247 omavirus, herpes virus) and bacterial (e.g., Helicobacter pylori, pneumonia) diseases, and autoimmune

248 Helicobacter pylori, the causative agent of gastric canc

249 Helicobacter pylori, the dominant member of the human ga

250 Helicobacter pylori, the main cause of peptic ulcer dise

251 Gram-negative bacteria, and in particular of Helicobacter pylori, the mechanisms underlying the handl

252 dies reported an association of the bacteria Helicobacter pylori, the primary cause of gastric cancer

253 tic distribution of human pathogens, such as Helicobacter pylori, thereby demonstrating the potential

254 oteins in the bacterial chemotaxis system of Helicobacter pylori, which requires two nonredundant cou

255 as being involved in the pathophysiology of Helicobacter pylori-associated diseases, the role of oth

256 The pathogenesis of Helicobacter pylori-associated gastric cancer is depende

257 n chronic inflammatory conditions, including Helicobacter pylori-associated gastritis, where its prod

258 he polymorphic CagA toxin is associated with Helicobacter pylori-induced disease.

259 Helicobacter pylori-induced gastritis is the strongest r

260 Helicobacter pylori-induced miR-135b-5p promotes cisplat

261 , gastric immunopathology was accelerated in Helicobacter pylori-infected Gkn2 knockout mice and was

262 proposed that the accompanying microbiota in Helicobacter pylori-infected individuals might affect di

263 ks (UC), vitamin D deficiency (IBD), and non-Helicobacter pylori-like enterohepatic Helicobacter spec

264 link is provided by the association between Helicobacter pylori-positive gastritis and gastric MALT

265 re commonly used as a first-line therapy for Helicobacter pylori-positive patients; however, resistan

266 ings behind the regulation of a type I TA in Helicobacter pylori.

267 s associated with tetracycline resistance in Helicobacter pylori.

268 rgy and infection with the gastric bacterium Helicobacter pylori.

269 ainst SK from Mycobacterium tuberculosis and Helicobacter pylori.

270 s has been questioned since the discovery of helicobacter pylori.

271 bacteria such as the human gastric pathogen Helicobacter pylori.

272 dy the epithelial response to infection with Helicobacter pylori.

273 main protein from the human gastric pathogen Helicobacter pylori.

274 uman papilloma virus, hepatitis C virus, and Helicobacter pylori.

275 was described as a chemotaxis attractant for Helicobacter pylori.

276 lation is infected with the stomach pathogen Helicobacter pylori.

277 h functional dyspepsia who test positive for Helicobacter pylori.

278 nic atrophic gastritis due to infection with Helicobacter pylori; it might be a precursor to intestin

279 own, whereby oxidant-stressed (HOCl-exposed) Helicobacter retained viability even upon extracellular

280 se-negative, fusiform, novel bacterium named Helicobacter saguini was isolated from the intestines an

281 This model using a nonhuman primate Helicobacter sp. can be used to study the pathogenic pot

282 Helicobacter sp. was detected in 69% of feces or intesti

283 rulence factors found in other enterohepatic helicobacter species (EHS) and H. pylori These include f

284 d non-Helicobacter pylori-like enterohepatic Helicobacter species (IBD).

285 e demonstrated that the introduction of both Helicobacter species activated ILCs and induced gut infl

286 oyl-ACP methyl ester esterase present in the Helicobacter species and their occurrence only in H. pyl

287 Enterohepatic Helicobacter species are associated with several digesti

288 t of gastric lymphoid infiltrates induced by Helicobacter species in vivo.

289 The CdtB of these Helicobacter species induced nuclear factor kappaB nucle

290 FP-based phylogenetic trees of seven gastric Helicobacter species matched those obtained by analysis

291 We believe that APRIL Tg mice infected by Helicobacter species may represent a novel animal model

292 and induced gut inflammation; however, these Helicobacter species negatively regulated RORgammat(+) g

293 We present a study of the infection by Helicobacter species of transgenic (Tg) C57BL6 mice, ect

294 eria to Bacteroidetes, decreased presence of Helicobacter species, and elevated representation of Muc

295 y unknown dichotomous regulation of ILC3s by Helicobacter species, and may serve as a model for furth

296 e identified opposing effects on ILCs by two Helicobacter species, Helicobacter apodemus and Helicoba

297 spensable for Mycobacterium, Salmonella, and Helicobacter species.

298 ated bacteria, such as Dysgonomonas spp. and Helicobacter spp., was profoundly lower in Rb3/Rd-treate

299 and aggravated gastric pathology induced by Helicobacter through activation of non-canonical NF-kapp

300 icobacter species, Helicobacter apodemus and Helicobacter typhlonius, isolated from immunocompromised