ライフサイエンスコーパス: gastric epithelial cell

1 e biological consequences of these events in gastric epithelial cells.

2 ri, vacA, induces cytoplasmic vacuolation in gastric epithelial cells.

3 teinase-dependent release of EGFR ligands in gastric epithelial cells.

4 ori-infected patients and in vitro using AGS gastric epithelial cells.

5 n internalization and barrier dysfunction in gastric epithelial cells.

6 totic genes, NOXA, PUMA, and FAS receptor in gastric epithelial cells.

7 transporter that is abundantly expressed in gastric epithelial cells.

8 CagA directly through the plasma membrane of gastric epithelial cells.

9 ndritic cells, macrophages, fibroblasts, and gastric epithelial cells.

10 lpAB reduced interleukin (IL)-6 induction in gastric epithelial cells.

11 hibit reduced ability to translocate CagA in gastric epithelial cells.

12 secretion system that translocates CagA into gastric epithelial cells.

13 gene expression in H. pylori-infected human gastric epithelial cells.

14 nd increases the expression of IL-8 in human gastric epithelial cells.

15 iously shown that H. pylori binds to CD74 on gastric epithelial cells.

16 he production of IL-18 from human and murine gastric epithelial cells.

17 ), which was found to be highly expressed by gastric epithelial cells.

18 chemoreceptor to sense signals generated by gastric epithelial cells.

19 histo-blood group antigen on the surface of gastric epithelial cells.

20 by inducing apoptosis and DNA damage in host gastric epithelial cells.

21 ioxidants on APE-1/Ref-1 expression in human gastric epithelial cells.

22 n and messenger RNA were detected in resting gastric epithelial cells.

23 nt to the site of bacterial adhesion on host gastric epithelial cells.

24 hanges in ADAM 10 and ADAM 17 transcripts in gastric epithelial cells.

25 overexpression in neoplastic but not normal gastric epithelial cells.

26 of a low level reservoir of H. pylori within gastric epithelial cells.

27 could regulate the response to H. pylori in gastric epithelial cells.

28 /2 phosphorylation in H. pylori-infected AGS gastric epithelial cells.

29 ri to induce NF-kappaB-mediated apoptosis in gastric epithelial cells.

30 amma modified H. pylori-induced apoptosis in gastric epithelial cells.

31 of H. pylori on mucin synthesis in cultured gastric epithelial cells.

32 d in the basolateral membrane and cytosol of gastric epithelial cells.

33 monoamine transporter 2 (VMAT2) promoter in gastric epithelial cells.

34 ensatory hyperproliferation by nonneoplastic gastric epithelial cells.

35 s mitogen-activated protein (MAP) kinases in gastric epithelial cells.

36 of an IL-8 cytokine inflammatory response in gastric epithelial cells.

37 ynthesis of proinflammatory cytokine IL-8 in gastric epithelial cells.

38 ria as well as the induction of apoptosis in gastric epithelial cells.

39 ivity, which elevates IL-8 expression in AGS gastric epithelial cells.

40 om H. pylori-infected AGS and Kato III human gastric epithelial cells.

41 uced through urease activity may be toxic to gastric epithelial cells.

42 6)A methylases and increases m(6)A levels in gastric epithelial cells.

43 ll as nonprotein bacterial constituents into gastric epithelial cells.

44 nfluence interleukin 8 secretion by the host gastric epithelial cells.

45 against acid injury and oxidative stress in gastric epithelial cells.

46 the capacity to induce interleukin (IL)8 in gastric epithelial cells.

47 changes that lead to genetic instability in gastric epithelial cells.

48 alpha-stimulated expression of IL8 in canine gastric epithelial cells.

49 isolates was analyzed during coculture with gastric epithelial cells.

50 ts monolayer permeability of polarized human gastric epithelial cells.

51 a cytotoxin generated by H pylori that kills gastric epithelial cells.

52 of HDM2 and subsequent degradation of p53 in gastric epithelial cells.

53 triggers activation of the COX-2 gene in rat gastric epithelial cells: action mediated through the ER

54 racellular Ca(2+) mobilization occurs within gastric epithelial cells adjacent to the damage site to

55 Ca(2+) selectively increases in restituting gastric epithelial cells adjacent to the damaged cells.

56 s and dendritic cells, as well as from human gastric epithelial cells (AGS cell line).

57 f Helicobacter pylori and shown to bind with gastric epithelial cells (AGS cells).

58 MKN45 gastric epithelial cells, AGS cells, and human primary g

59 ted by a type 4 secretion system (T4SS) into gastric epithelial cells and activates oncogenic signali

60 uce gastric injury by mediating adherence to gastric epithelial cells and by modulating proinflammato

61 nd chemoreceptor mutants adhered to cultured gastric epithelial cells and caused cellular release of

62 . pylori both increased apoptosis in primary gastric epithelial cells and decreased phagocytosis of t

63 The cagA gene product CagA is injected into gastric epithelial cells and disturbs cellular functions

64 er pylori translocates the protein CagA into gastric epithelial cells and has been linked to peptic u

65 synthesis and nuclear accumulation in human gastric epithelial cells and implicate APE-1/Ref-1 in th

66 n on the DNA damage response sensor, ATM, in gastric epithelial cells and in biopsy specimens from pa

67 lobal DNA methylation both in the dysplastic gastric epithelial cells and in gastric stromal myofibro

68 n contrast, hBD-2 expression is regulated in gastric epithelial cells and increases in response to in

69 contrast to the spiral form, binds poorly to gastric epithelial cells and induces little, if any, int

70 H. pylori binds to class II MHC molecules on gastric epithelial cells and induces their apoptosis.

71 ction by increasing the expression of Fas on gastric epithelial cells and inducing apoptosis through

72 t impaired in its ability to deliver CagA to gastric epithelial cells and initiate cell elongation.

73 er that is active in a rare subpopulation of gastric epithelial cells and investigated whether these

74 osal biopsy specimens as well as in isolated gastric epithelial cells and lamina propria mononuclear

75 Infection increased cytokine production from gastric epithelial cells and macrophages and elevations

76 Primary gastric epithelial cells and MKN28 cells were cocultured

77 , how NO and H. pylori interact to signal in gastric epithelial cells and modulate the innate immune

78 Prolonged exposure of human gastric epithelial cells and mouse gastric cells to VacA

79 ted the effect of VacA on autophagy in human gastric epithelial cells and primary gastric cells from

80 airpin RNA (shRNA) libraries in AZ-521 human gastric epithelial cells and selected for VacA-resistant

81 Helicobacter pylori adheres to gastric epithelial cells and stimulates interleukin (IL)

82 an stomach by causing programmed necrosis of gastric epithelial cells and subsequent release of proin

83 e factor that causes multiple alterations in gastric epithelial cells and T cells.

84 i secretes a toxin, VacA, that targets human gastric epithelial cells and T lymphocytes and enhances

85 cyte-macrophage colony-stimulating factor by gastric epithelial cells and that these molecules induce

86 We investigated how cgt affects gastric epithelial cells and the host immune response.

87 We also investigated IL-18 levels in gastric epithelial cells and the monocyte cell line THP-

88 To address the fate of apoptotic gastric epithelial cells and their role in H. pylori muc

89 f cgt reduces cholesterol levels in infected gastric epithelial cells and thereby blocks IFNG signali

90 ndin synthesizing enzyme, cyclooxygenase) in gastric epithelial cells and whether this action is medi

91 ion is disrupted in elf+/- / Smad4+/- mutant gastric epithelial cells, and could be rescued by ectopi

92 levels of SMO, apoptosis, and DNA damage in gastric epithelial cells, and knockdown or inhibition of

93 lized at the interface between H. pylori and gastric epithelial cells, and previous studies suggested

94 determine the function of these molecules on gastric epithelial cells, antibodies to B7-1 and B7-2 we

95 clooxygenase may perturb the balance between gastric epithelial cell apoptosis (ulcer formation) and

96 These results indicate that VacA induces gastric epithelial cell apoptosis and suggest that diffe

97 hesis that there is a relative deficiency of gastric epithelial cell apoptosis associated with the ca

98 H pylori infection stimulated gastric epithelial cell apoptosis in EGFRwa2 but not in

99 H. pylori vacuolating toxin (VacA) to induce gastric epithelial cell apoptosis.

100 Other gastric epithelial cells appeared normal.

101 disintegrin and metalloproteinase) genes in gastric epithelial cells are differentially expressed af

102 the current study, we show that AZ-521 human gastric epithelial cells are highly susceptible to VacA-

103 Since human gastric epithelial cells are readily available from dono

104 critical role of the 3'SL structure on human gastric epithelial cells as an adherence ligand for rece

105 tively little effect on the viability of AGS gastric epithelial cells, but the presence of exogenous

106 to H. pylori's ability to delay apoptosis in gastric epithelial cells by actively driving the degrada

107 expression was detected on freshly isolated gastric epithelial cells by flow cytometry and immunohis

108 Infection of gastric epithelial cells by H. pylori triggers an autocr

109 Knockdown of Muc1 expression in AGS human gastric epithelial cells by RNA interference was associa

110 The transport of the CagA effector into gastric epithelial cells by the Cag Type IV secretion sy

111 pylori directly contributes to the injury of gastric epithelial cells by the elaboration of cytotoxic

112 NF-kappa B activation was decreased in MKN45 gastric epithelial cells by transfection of dominant-neg

113 y activates ERK, p38, and JNK MAP kinases in gastric epithelial cells; cag+ isolates are more potent

114 However, apart from immune cells, gastric epithelial cells can also produce IL-18.

115 on, the expression of mutant K-ras in K19(+) gastric epithelial cells can induce chronic inflammation

116 Attachment of the bacterium to polarized gastric epithelial cells causes damage to microvilli and

117 lori up-regulates spermine oxidase (SMOX) in gastric epithelial cells, causing oxidative stress-induc

118 eceptor proteins in solubilized membranes of gastric epithelial cells, class II major histocompatibil

119 When cocultured with gastric epithelial cells, clinical strains of H. pylori

120 by immunohistochemistry and in H. pylori/AGS gastric epithelial cell coculture supernatants by Wester

121 sms of the p27 decrease, using AGS and MKN28 gastric epithelial cells cocultured with H. pylori strai

122 Similar data were also observed in primary gastric epithelial cells confirming the results obtained

123 ression levels of ST6GAL-I and SOX9 in human gastric epithelial cells correlated positively with one

124 gastric adenocarcinoma, possibly by altering gastric epithelial cell cycle events and/or gastrin secr

125 ost response interact in the pathogenesis of gastric epithelial cell damage.

126 on of ODC activity or ODC knockdown in human gastric epithelial cells dampens H. pylori-induced NF-ka

127 Laser capture microdissection of human gastric epithelial cells demonstrated expression of SMO(

128 for normal levels of gastric acid secretion, gastric epithelial cell differentiation, and development

129 Shh (Sonic hedgehog) regulates gastric epithelial cell differentiation.

130 s mediating the actions of growth factors on gastric epithelial cell differentiation.

131 Transactivation of gastric epithelial cell EGF receptors may be instrumenta

132 otype when naive T cells were incubated with gastric epithelial cells exposed to H. pylori.

133 e transcriptase-PCR we determined that MKN45 gastric epithelial cells express low but detectable amou

134 T cells, it was important to establish human gastric epithelial cells expressed those surface ligands

135 In 34 specimens, residual normal gastric epithelial cells (foveolar cells) were present f

136 is a gastric tumor suppressor that protects gastric epithelial cells from damage but can promote inv

137 , apoptosis, and DNA damage were measured in gastric epithelial cells from H. pylori-infected Egfr(wa

138 Similarly, B7-2 expression was higher on gastric epithelial cells from H. pylori-infected tissues

139 ore, HpGroES-induced IL-8 release by primary gastric epithelial cells from TLR4(-/-) mice was signifi

140 ntify mechanisms by which Shh might regulate gastric epithelial cell function and differentiation.

141 Helicobacter pylori-induced gastric epithelial cell (GEC) apoptosis is a complex pro

142 own to be highly expressed on the surface of gastric epithelial cells (GEC) during H. pylori infectio

143 Gastric epithelial cells (GEC) play an important role du

144 osis and increases APE-1 expression in human gastric epithelial cells (GEC).

145 ce with a conditional knockout of IKKbeta in gastric epithelial cells (GECs) and myeloid cells, and e

146 Gastric epithelial cells (GECs) are the primary target f

147 arcinogenic mechanisms and is upregulated on gastric epithelial cells (GECs) during H. pylori exposur

148 Gastric epithelial cells (GECs) express the class II maj

149 ter Helicobacter pylori infection in humans, gastric epithelial cells (GECs) undergo apoptosis due to

150 Absence of RUNX3 expression from normal gastric epithelial cells (GECs), the progenitors to GC,

151 tein myeloid cell leukemia 1 (Mcl1) in human gastric epithelial cells (GECs).

152 901), but less cytotoxicity to non-malignant gastric epithelial cells GES1.

153 protein (BMP) signaling in the regulation of gastric epithelial cell growth and differentiation by ge

154 Moreover, during infection of gastric epithelial cells, H. pylori induce intracellular

155 In cultured gastric epithelial cells, H. pylori induced transcriptio

156 When cocultured with AGS gastric epithelial cells, H. pylori strain 60190, which

157 dings suggest that promoting the survival of gastric epithelial cells has implications not only for H

158 Both cultured gastric epithelial cells (HFE145 and NCI-N87) and primar

159 BMPs are therefore important regulators of gastric epithelial cell homeostasis.

160 cells in the stomach and the maintenance of gastric epithelial cell identity.

161 nvestigated phagocyte clearance of apoptotic gastric epithelial cells in H. pylori infection.

162 facilitates anchorage-independent growth of gastric epithelial cells in soft agar.

163 In vivo, MMP-7 was expressed in gastric epithelial cells in specimens from 80% of cag(+)

164 Gastric epithelial cells in vitro and in vivo are shown

165 selectively increase MMP-7 protein levels in gastric epithelial cells in vitro and in vivo.

166 H. pylori infection activates NF-kappa B in gastric epithelial cells in vitro and in vivo.

167 acute mucosal inflammation, and adherence to gastric epithelial cells in vitro induces expression of

168 H. pylori stimulates expression of MMP-7 in gastric epithelial cells in vitro.

169 ional organoids, modelling the plasticity of gastric epithelial cells in vivo.

170 xin, VacA, can cause multiple alterations in gastric epithelial cells, including cell death.

171 variety of phenotypic responses in cultured gastric epithelial cells, including the expression of pr

172 e factor CagA; ectopic expression of CagA in gastric epithelial cells increased phosphorylation of HD

173 chanisms leading to upregulation of MMP10 in gastric epithelial cells induced by H. pylori Infection

174 We then used primary human gastric epithelial cells induced to undergo apoptosis by

175 Of note, CRISPR deletion of CBS in normal gastric epithelial cells induces widespread DNA methylat

176 zed by an abundant inflammatory response and gastric epithelial cell injury.

177 platform for advancing our understanding of gastric epithelial cell interactions, gastric mucosal im

178 Following adhesion of Helicobacter pylori to gastric epithelial cells, intracellular signaling leads

179 c Ca(2+) mobilization within the restituting gastric epithelial cells is a central signal driving sma

180 Increased apoptotic death of gastric epithelial cells is a hallmark of Helicobacter p

181 Adherence of Helicobacter pylori to cultured gastric epithelial cells is associated with several cell

182 astric cancer, and adherence of H. pylori to gastric epithelial cells is critical for induction of in

183 process for which adherence of H. pylori to gastric epithelial cells is critical.

184 -8; however, the mechanism(s), especially in gastric epithelial cells, is not well understood.

185 Interaction of H pylori with gastric epithelial cells leads to robust up-regulation o

186 Gastric epithelial cells liberate prostaglandin E(2) in

187 EGF on PKC, Ras, and ERK activities in a rat gastric epithelial cell line (RGM1).

188 In addition, the CXCR4-negative gastric epithelial cell line AGS became highly responsiv

189 Adherence of Helicobacter pylori to the gastric epithelial cell line AGS strongly induces expres

190 Adherence of Helicobacter pylori to the gastric epithelial cell line AGS strongly upregulated ex

191 transcriptomes of mGEPs and a control mouse gastric epithelial cell line revealed that, upon infecti

192 Treatment of the rat gastric epithelial cell line RGM1 with transforming grow

193 study, we show that in vitro infection of a gastric epithelial cell line with EBV alters growth prop

194 stomach epithelial cells (ImSt) and a human gastric epithelial cell line, AGS cells, as well as wild

195 ut (IFN-gamma(-/-)) mouse model and a murine gastric epithelial cell line, GSM06, we demonstrated tha

196 s markers associated with differentiation of gastric epithelial cell lineages.

197 ssion of B7-1 and B7-2 was detected on human gastric epithelial cell lines and freshly isolated epith

198 its receptors in vivo and with a variety of gastric epithelial cell lines during infection with H. p

199 DNA damage (8-oxoguanosine) were measured in gastric epithelial cell lines infected with cagA(+) or c

200 Human gastric epithelial cell lines or cells isolated from muc

201 mma was expressed and functionally active in gastric epithelial cell lines sensitive to H. pylori-ind

202 The role of Fas in apoptosis of gastric epithelial cell lines was evidenced by DNA fragm

203 The expression of Fas receptor on three gastric epithelial cell lines was increased by H. pylori

204 ma, which increases class II MHC expression, gastric epithelial cell lines were exposed to H. pylori

205 ssion and promoter methylation status in six gastric epithelial cell lines.

206 ing of PE-conjugated urease to class II MHC+ gastric epithelial cell lines.

207 tissues, as well as in GC-derived and normal gastric epithelial cell lines.

208 s, and inflammatory responses, activation of gastric epithelial cell MAP kinases by H. pylori cag+ st

209 ue injury, we asked whether MMP secretion by gastric epithelial cells may contribute to gastric injur

210 upregulation of PAI-1 in H. pylori-infected gastric epithelial cells may contribute to the carcinoge

211 We found that interaction of H. pylori with gastric epithelial cells, mediated via the cag pathogeni

212 urine model results in greater disruption of gastric epithelial cell morphology, increased gastric ce

213 We show increased isoLG adducts in gastric epithelial cell nuclei in patients with gastriti

214 ithelial cells, AGS cells, and human primary gastric epithelial cells (obtained from patients undergo

215 The effect of EtHOBA on mutations in gastric epithelial cells of H pylori-infected INS-GAS mi

216 ith these findings, HO-1 is downregulated in gastric epithelial cells of patients infected with cagA(

217 s infected with cagA(+) H. pylori but not in gastric epithelial cells of patients infected with cagA(

218 region of p65 showed activated NF-kappa B in gastric epithelial cells of patients with H. pylori gast

219 nate TAS2Rs for caffeine, was shown in human gastric epithelial cells of the corpus/fundus and in HGT

220 Unusually for normal cells, gastric epithelial cells often carry recurrent trisomies

221 (gp130) receptor in inflammation-associated gastric epithelial cell oncogenic transformation, which

222 Gastric epithelial cells or colonies were co-cultured wi

223 wever, its role has not been investigated in gastric epithelial cells or gastric tumorigenesis.

224 7.13 or its pgdA(-) isogenic mutant with AGS gastric epithelial cells or HEK293 epithelial cells expr

225 owever, the mechanism by which CagA disrupts gastric epithelial cell polarity to achieve its oncogeni

226 fection would lead to increased apoptosis of gastric epithelial cells, possibly in response to free r

227 position to influence decision-making among gastric epithelial cell precursors and to modulate the m

228 pylori urease B subunit to CD74 expressed on gastric epithelial cells presents a novel insight into a

229 sults may explain heterogeneity in levels of gastric epithelial cell proliferation and apoptosis foun

230 ylori infection disrupts the balance between gastric epithelial cell proliferation and apoptosis, whi

231 Helicobacter pylori cag+ strains enhance gastric epithelial cell proliferation and attenuate apop

232 -catenin, p120, and PPARdelta, which promote gastric epithelial cell proliferation via activation of

233 These studies demonstrate that gastric epithelial cells recognize and respond to H. pyl

234 The mechanisms through which gastric epithelial cells recognize this organism are unc

235 fic deletion of the gene encoding for ODC in gastric epithelial cells reduces gastritis, attenuates e

236 carcinogenesis, how H. pylori reduces p27 in gastric epithelial cells remains unknown.

237 lts indicate that attachment of H. pylori to gastric epithelial cells resembles that of enteropathoge

238 t hBD-2 is a component of the regulated host gastric epithelial cell response to H. pylori infection

239 epithelial damage site that are essential to gastric epithelial cell restitution in vivo.

240 the monitoring of Ca(2+) mobilization during gastric epithelial cell restitution.

241 , and enzyme activity of SMO(PAOh1) in human gastric epithelial cells, resulting in DNA damage and ap

242 cs, cell migration, and proliferation in rat gastric epithelial cell (RGM1) and smooth muscle cell (A

243 Adherence of H. pylori to gastric epithelial cells seems to be required for bacter

244 n understanding the role of CagA in altering gastric epithelial cell signaling pathways.

245 ortant lipo-polysaccharide (LPS) receptor in gastric epithelial cell signaling transduction and plays

246 oids or chemical inhibition of SMOX in human gastric epithelial cells significantly reduced generatio

247 emperature requirement A (HtrA) that cleaves gastric epithelial cell surface proteins to disrupt the

248 ori infection has an antiapoptotic effect in gastric epithelial cells that appears to involve Akt sig

249 mmatory response and oxidative DNA damage in gastric epithelial cells that can lead to gastric cancer

250 Recombinant urease induced apoptosis in gastric epithelial cells that express class II MHC molec

251 decrease in p53 levels increased survival of gastric epithelial cells that had sustained DNA damage.

252 A/A increased Ca(2+) permeation in gastric epithelial cells; the increase was blocked by NM

253 H. pylori induces DAF expression in human gastric epithelial cells; therefore, we sought to define

254 ammatory effector heme oxygenase-1 (HO-1) in gastric epithelial cells through a pathway that requires

255 ter pylori CagA protein is translocated into gastric epithelial cells through a type IV secretion sys

256 factor that Helicobacter pylori inject into gastric epithelial cells through a type IV secretion sys

257 IFN-gamma also induced autophagy in gastric epithelial cells through increased expression of

258 HGF triggers activation of the COX-2 gene in gastric epithelial cells through phosphorylation of c-Me

259 bacter pylori causes numerous alterations in gastric epithelial cells through processes that are depe

260 ction, and may enhance the susceptibility of gastric epithelial cells to carcinogenic conversion.

261 Exposure of gastric epithelial cells to the bacterial carcinogen Hel

262 ter and ADAM17 activity were measured in AGS gastric epithelial cells transfected with HKalpha promot

263 described bacterial oncoprotein, CagA causes gastric epithelial cell transformation by promoting an e

264 ylori infection is associated with increased gastric epithelial cell turnover and is a risk factor fo

265 Gastric epithelial cell turnover was no different after

266 pylori infection is associated with altered gastric epithelial cell turnover.

267 reatment led to the reemergence of all major gastric epithelial cell types and restoration of glandul

268 ulation of intracellular pH in each of these gastric epithelial cell types.

269 In vitro studies in gastric epithelial cells using dupA -deleted and -comple

270 Interactions between CagL and host gastric epithelial cell via integrins are required for t

271 H. pylori CagA is translocated into gastric epithelial cells via a type IV secretion pathway

272 A/A affects gastric epithelial cell viability by allowing excessive

273 Additionally, acrolein-induced DNA damage in gastric epithelial cells was ablated with the electrophi

274 at the HpGroES-induced IL-8 release by human gastric epithelial cells was dependent on activation of

275 l and H. pylori -infected gastric mucosa and gastric epithelial cells was determined by in situ hybri

276 of this molecule in adhesion of H. pylori to gastric epithelial cells was investigated.

277 The binding of urease to human gastric epithelial cells was reduced by anti-class II MH

278 Gastric epithelial cells were co-cultured with H pylori

279 Gastric epithelial cells were cocultured with Helicobact

280 MKN28 gastric epithelial cells were cocultured with the H pylo

281 AGS gastric epithelial cells were cultured alone or in the p

282 Gastric epithelial cells were cultured to confluence and

283 the role of oxidative stress in cell death, gastric epithelial cells were exposed to various strains

284 AGS gastric epithelial cells were infected with cag(+) toxig

285 Gastric epithelial cells were isolated from the entire s

286 se this receptor as a point of attachment to gastric epithelial cells, which lead to IL-8 production.

287 g cytotoxin (VacA) inhibits proliferation of gastric epithelial cells, which suggests that H pylori m

288 , also caused extensive Ca(2+) permeation of gastric epithelial cells, which was blocked when NMDA-re

289 nt expression and activation of PPARdelta in gastric epithelial cells, which were mediated by the cag

290 Infection of cultured gastric epithelial cells with a wild-type but not an iso

291 Gastric epithelial cells with DNA damage that were negat

292 Coculture of gastric epithelial cells with H. pylori grown under high

293 Experimental coculture of gastric epithelial cells with the strains containing the

294 Co-culture of MKN28 gastric epithelial cells with the wild-type H. pylori ca

295 We co-cultured gastric epithelial cells with wild type H. pylori strain

296 By in vitro infection of gastric epithelial cells with wild-type and VacA-deficie

297 We cocultured gastric epithelial cells with wild-type H. pylori, isoge

298 R-spondins are critical regulators of gastric epithelial cells, with Lgr5 receptor historicall