ライフサイエンスコーパス: bronchial epithelial cell

1 e (CpG) resolution global DNA methylation in bronchial epithelial cells.

2 naria extract-induced IL-33 release by human bronchial epithelial cells.

3 trap beta1-integrins on the luminal pole of bronchial epithelial cells.

4 n cigarette smoke-exposed mice, and in human bronchial epithelial cells.

5 ible activation of oncogenes in immortalized bronchial epithelial cells.

6 as well as malignant transformation of human bronchial epithelial cells.

7 3O-C12-HSL attenuate PPARgamma expression in bronchial epithelial cells.

8 hese CREs from the endogenous locus in human bronchial epithelial cells.

9 ecreted exosomes, which were internalized by bronchial epithelial cells.

10 as biofilms on the Cystic Fibrosis genotype bronchial epithelial cells.

11 sulting in malignant transformation of human bronchial epithelial cells.

12 ced miR-132-3p may contribute to shedding of bronchial epithelial cells.

13 red by diesel particles or allergen in human bronchial epithelial cells.

14 in vitro transfecting miRNA mimics in human bronchial epithelial cells.

15 ains in the plasma membrane of primary human bronchial epithelial cells.

16 oscopy did not show spore internalization by bronchial epithelial cells.

17 otherwise resistant telomerase-immortalized bronchial epithelial cells.

18 chemical stimuli, given the responses in rat bronchial epithelial cells.

19 ospho-SMAD2/3 and ZEB-2 in cultures of human bronchial epithelial cells.

20 -induced SMAD signaling in cultures of human bronchial epithelial cells.

21 rneal epithelial cells and insulin-sensitive bronchial epithelial cells.

22 replication and impaired TLR3 expression in bronchial epithelial cells.

23 level of GAB1 after GC treatment in BEAS-2B bronchial epithelial cells.

24 to cigarette smoke-induced transformation of bronchial epithelial cells.

25 B replicates to lower levels also in primary bronchial epithelial cells.

26 upstream pro-allergic cytokine, in asthmatic bronchial epithelial cells.

27 ependent activation of CFTR in primary human bronchial epithelial cells.

28 tein expression of TRPV1 in cultured primary bronchial epithelial cells.

29 particulate matter (PMMTM) exposure on human bronchial epithelial cells.

30 atory epithelial cell line and primary human bronchial epithelial cells.

31 SLC22A15 as being expressed in the lung and bronchial epithelial cells.

32 istal source of Fgf10 and differentiate into bronchial epithelial cells.

33 internalization of Haemophilus influenzae in bronchial epithelial cells.

34 ced interferon-beta and interferon-lambda in bronchial epithelial cells.

35 o barrier dysfunction and cell activation in bronchial epithelial cells.

36 sion of YEATS4 abrogated senescence in human bronchial epithelial cells.

37 eading edge of polarized and migrating human bronchial epithelial cells.

38 lung cancer cells compared with normal human bronchial epithelial cells.

39 lls with primary differentiated normal human bronchial epithelial cells.

40 ) as well as in primary human astrocytes and bronchial epithelial cells.

41 tide S100A7 and epithelial cell migration in bronchial epithelial cells.

42 motes binding of NTHi to laminin and primary bronchial epithelial cells.

43 ntified variants was conducted using primary bronchial epithelial cells.

44 ) that are predicted to target CFTR in human bronchial epithelial cells.

45 a, TNF-alpha, T(H)1 cells, and rhinovirus in bronchial epithelial cells.

46 or the first time that nickel induces EMT in bronchial epithelial cells.

47 sly established for culture of primary human bronchial epithelial cells.

48 miRNA-200b in TGF-beta1-induced EMT in human bronchial epithelial cells.

49 increase mucin expressions in primary human bronchial epithelial cells.

50 e chloride channel activity in primary human bronchial epithelial cells.

51 omolecular complexes at the surface of human bronchial epithelial cells.

52 target gene expression in mice and in human bronchial epithelial cells.

53 pEMT) or UJT in differentiated primary human bronchial epithelial cells.

54 cells, such as interstitial macrophages and bronchial epithelial cells.

55 replicated selected findings in normal human bronchial epithelial cells.

56 l cell culture of fully differentiated human bronchial epithelial cells.

57 induced goblet cell differentiation of human bronchial epithelial cells.

58 suppression rescues F508del-CFTR function in bronchial epithelial cells.

59 mouse embryonic fibroblasts and normal human bronchial epithelial cells.

60 vivo murine model of COPD, and primary human bronchial epithelial cells.

61 icant mitochondrial superoxide production in bronchial epithelial cells (16-HBE).

62 Similarly, human bronchial epithelial cell (16HBE) lysates metabolized HO

63 tested for potential cytotoxicity to a human bronchial epithelial cell, 16HBE14o-.

64 genomes of 632 colonies derived from single bronchial epithelial cells across 16 subjects.

65 h levels and higher, are toxic for the human bronchial epithelial cells after 4-day exposure.

66 se activity and strong ability in protecting bronchial epithelial cells against elastase-induced anti

67 up-regulates NeuroD1 in immortalized normal bronchial epithelial cells and a subset of undifferentia

68 ntiinflammatory therapy in CF using CF human bronchial epithelial cells and an ovine model of CF-like

69 om bleomycin-induced apoptosis using primary bronchial epithelial cells and BEAS-2B cells.

70 hingosine is present in nasal, tracheal, and bronchial epithelial cells and constitutes a central ele

71 A damage potential of aeroallergens on human bronchial epithelial cells and elucidated the mechanisms

72 degrees C, we studied RV infection in human bronchial epithelial cells and H1-HeLa cells.

73 anilloid-3 (TRPV3) agonists can affect human bronchial epithelial cells and highlight novel physiolog

74 . aureus to the intracellular niche in human bronchial epithelial cells and in a murine pneumonia mod

75 ucociliary parameters were measured in human bronchial epithelial cells and in sheep.

76 ed increased expression of MMP-10 and MET in bronchial epithelial cells and in subepithelial inflamma

77 A biculture of human bronchial epithelial cells and lung microvascular endoth

78 nducted in two human cell lines representing bronchial epithelial cells and macrophages and female mi

79 mulation on barrier function of normal human bronchial epithelial cells and nasal epithelial cells cu

80 type I and III interferon response to TLR in bronchial epithelial cells and peripheral blood cells fr

81 d TLR7/8,, stimulation induced interferon in bronchial epithelial cells and peripheral blood mononucl

82 Bronchial epithelial cells and peripheral blood mononucl

83 Mucin 1-CT expression was downregulated in bronchial epithelial cells and peripheral blood neutroph

84 ted allergen-induced PGE2 secretion in human bronchial epithelial cells and prostanoid-dependent bron

85 elicit innate immune responses in both human bronchial epithelial cells and pulmonary microvascular e

86 ypes, and pathway analysis were performed in bronchial epithelial cells and replicated.

87 a natural rodent pathogen that replicates in bronchial epithelial cells and reproduces many clinical

88 recently shown that ex-vivo cultured primary bronchial epithelial cells and the bronchial brushings f

89 miR-200b was expressed in bronchial epithelial cells and vascular endothelial cell

90 of wild-type VN1203 in MDCK and normal human bronchial epithelial cells and yet had reduced growth in

91 ded with drugs in vitro (normal and CF human bronchial epithelial cells) and in vivo (homozygote/homo

92 lung epithelial cells (alveolar type II and bronchial epithelial cells), and two different cell type

93 lating DSP (desmoplakin) expression in human bronchial epithelial cells, and DSP regulates extracellu

94 expression by dexamethasone in primary human bronchial epithelial cells, and in A549 cells IL1B-induc

95 ne expression, Nrf2 nuclear translocation in bronchial epithelial cells, and increased reduced glutat

96 USPs 1, 4, and 10) were expressed in primary bronchial epithelial cells, and one of them, DUSP10, was

97 uses were also characterized in normal human bronchial epithelial cells, and the results were consist

98 ysLTr1(-/-) mice also demonstrated prolonged bronchial epithelial cell apoptosis following Cl2 WT mic

99 R pathways by Tet1 was also present in human bronchial epithelial cells at base line and following HD

100 tent in inducing mdig protein and/or mRNA in bronchial epithelial cells, B cells and MM cell lines.

101 mimicked using a novel differentiated bovine bronchial epithelial cell (BBEC) infection model.

102 Human bronchial epithelial cells, BEAS-2B, directly exposed to

103 ican production, we studied an ex vivo human bronchial epithelial cell (BEC)/human lung fibroblast (H

104 Human bronchial epithelial cells (BEC) were isolated by bronch

105 fter lung transplantation (LTx) results from bronchial epithelial cell (BECs) damages, thought to be

106 We report induction of SOCS1 in bronchial epithelial cells (BECs) by asthma exacerbation

107 o determine whether ex vivo RSV infection of bronchial epithelial cells (BECs) from children with ast

108 Bronchial epithelial cells (BECs) produce CC chemokines,

109 with the supernatants of rhinovirus-infected bronchial epithelial cells (BECs) to assess type 2 cytok

110 ecombination in alveolar macrophages (AMFs), bronchial epithelial cells (BECs), and alveolar epitheli

111 focus on the role of GRHL2 in primary human bronchial epithelial cells, both as undifferentiated pro

112 Most isolates replicated in mice and human bronchial epithelial cells, but replication in swine tis

113 DEP and ambient PM, upregulate TSLP in human bronchial epithelial cells by a mechanism that includes

114 nd 3O-C12-HSL induce barrier derangements in bronchial epithelial cells by lowering the expression of

115 , and BK activity in fully differentiated CF bronchial epithelial cells by reducing mRNA expression o

116 plasma from 48 CF patients and in primary CF bronchial epithelial cells (CF-HBEC).

117 Primary human bronchial epithelial cells cultured in air-liquid interf

118 duced by insulin deprivation in normal human bronchial epithelial cells cultured in organotypic condi

119 sed on well-differentiated pediatric primary bronchial epithelial cell cultures (WD-PBECs) that mimic

120 ator efficacy was confirmed in primary human bronchial epithelial cell cultures generated from a N130

121 effects on RV-16-induced NF-kB activation in bronchial epithelial cell cultures.

122 are fit based on the available data on human bronchial epithelial cell cultures.

123 2 cytokines in WT mice and in primary human bronchial epithelial cell cultures.

124 hat reduced levels of CARMA3 in normal human bronchial epithelial cells decreases the production of p

125 r-liquid interface cultures of primary human bronchial epithelial cells derived from non-asthmatic do

126 sis of HMPV replication and transcription in bronchial epithelial cell-derived immortal cells was per

127 g path on regulation of primary normal human bronchial epithelial cell-derived matrix metalloproteina

128 In contrast, NuLi-1 immortalized human bronchial epithelial cells did express STING, which was

129 l mucosal production of IL-17A which acts on bronchial epithelial cells directly and in concert with

130 okine data derived from normal human and rat bronchial epithelial cells exposed in parallel to 52 dif

131 Primary cultures of normal human bronchial epithelial cells exposed to CigS exhibit decre

132 ctivity was decreased by 68% in normal human bronchial epithelial cells exposed to plasma from smoker

133 Using primary human bronchial epithelial cells exposed to smoke-concentrated

134 f protein phosphorylation responses in human bronchial epithelial cells, exposed to a number of diffe

135 In vitro primary bronchial epithelial cells expressed ST2 and IL-33 stimu

136 airway epithelial cells and developed human bronchial epithelial cells expressing Foxa3.

137 n a dose- and time-dependent manner in human bronchial epithelial cells following IR.

138 t epigenetic alterations can sensitize human bronchial epithelial cells for transformation by a singl

139 In human bronchial epithelial cells, formoterol, a long-acting be

140 zole increased chloride conductance in human bronchial epithelial cells from a DeltaF508 homozygous s

141 Primary human bronchial epithelial cells from asthma patients and cont

142 SCD1 expression was suppressed in bronchial epithelial cells from asthma patients.

143 enhanced and localization differed in human bronchial epithelial cells from asthmatic volunteers com

144 feron-lambda production has been reported in bronchial epithelial cells from asthmatics but the mecha

145 t, only a few viral antigens are detected in bronchial epithelial cells from autopsied lung sections.

146 Human bronchial epithelial cells from healthy and asthmatic su

147 internalization by SPX-101 in primary human bronchial epithelial cells from healthy and CF donors wa

148 Cultured primary bronchial epithelial cells from patients with mild asthm

149 Ex vivo, bronchial epithelial cells from people with asthma are m

150 Here we report that the transfer of human bronchial epithelial cells from stiff to soft substrates

151 Bronchial epithelial cells from the transplanted lung ca

152 Differentiated primary human bronchial epithelial cells from volunteers with and with

153 sive NF-kappaB signalling in resting primary bronchial epithelial cells from ZZ patients compared wit

154 These findings show that bronchial epithelial cell gene expression, as related to

155 er, whether endogenous expression in primary bronchial epithelial cells has similar consequences rema

156 Human bronchial epithelial cells (HBE) obtained from normal, n

157 effect of increased IL33 expression on human bronchial epithelial cell (HBEC) function.

158 Long-term exposure to arsenic causes human bronchial epithelial cell (HBEC) malignant transformatio

159 compared signaling changes across six human bronchial epithelial cell (HBEC) strains that were syste

160 sion was evaluated by real-time PCR in human bronchial epithelial cells (HBEC) and blood neutrophils

161 uced by transformation of immortalized human bronchial epithelial cells (HBEC) by expression of K-Ras

162 Here, data from human bronchial epithelial cells (HBEC) confirm that cigarette

163 ts within the lower airways to examine human bronchial epithelial cells (HBEC) is essential for under

164 6)-POB-dG repair in human lung, normal human bronchial epithelial cells (HBEC) were treated with mode

165 lignant lung cancer wherein we treated human bronchial epithelial cells (HBEC) with low doses of toba

166 n airway cell culture systems: primary human bronchial epithelial cells (HBEC), primary type II alveo

167 obal proteome analysis of immortalized human bronchial epithelial cells (HBEC3-KT) at day 7 post expo

168 we modeled malignant transformation in human bronchial epithelial cells (HBECs) and determined that E

169 d that LZTFL1 is expressed in ciliated human bronchial epithelial cells (HBECs) and its expression co

170 d 5-20-fold in hTERT/CDK4-immortalized human bronchial epithelial cells (HBECs) before treatment with

171 tures of control and asthmatic primary human bronchial epithelial cells (HBECs) by means of analysis

172 eved 30%-50% allelic correction in UABCs and bronchial epithelial cells (HBECs) from 10 CF patients a

173 We used primary human bronchial epithelial cells (HBECs) from asthmatics and h

174 nd negates scuPAR's effects on primary human bronchial epithelial cells (HBECs) in vitro.

175 culum stress (ERS) and cytotoxicity in human bronchial epithelial cells (HBECs) treated with pneumoto

176 Telomerase immortalized human bronchial epithelial cells (HBECs) with shTP53 and mutan

177 lysosomal organization in immortalized human bronchial epithelial cells (HBECs).

178 In BAL and bronchial epithelial cells, IL-26 increased gene express

179 In normal human bronchial epithelial cells, IL-8 secretion in response t

180 ial cells (BEAS-2B) and normal primary human bronchial epithelial cells in a concentration-dependent

181 ation and increased mucus viscosity of human bronchial epithelial cells in a nicotine-dependent manne

182 entiated CSE-induced transformation of human bronchial epithelial cells in a TNF-alpha-dependent mann

183 Gene expression studies of bronchial epithelial cells in individuals with asthma ha

184 e cytokines such as CXCL8 from human primary bronchial epithelial cells in response to RV-1B, without

185 as expressed by interstitial macrophages and bronchial epithelial cells in the inflamed lung, suggest

186 ce a pro-inflammatory state of senescence in bronchial epithelial cells in vitro and potentially in v

187 Here, we show that NTHI invades human bronchial epithelial cells in vitro in a lipid raft-inde

188 Transfection of ORMDL3 in human bronchial epithelial cells in vitro induced expression o

189 f FOXO transcription factors in alveolar and bronchial epithelial cells in vivo.

190 diate MNGC formation of vein endothelial and bronchial epithelial cells, indicating that the T6SS-5 i

191 effects of Th2 cytokines (IL-4 and IL-13) on bronchial epithelial cell innate immune antiviral respon

192 on was negatively regulated by PP2A in human bronchial epithelial cells isolated from healthy nonsmok

193 iven epithelial to mesenchymal transition in bronchial epithelial cells isolated from lung transplant

194 mucociliary function in differentiated human bronchial epithelial cells isolated from never-smokers a

195 nal proximal tubular epithelial cells, human bronchial epithelial cells, isolated intrahepatic biliar

196 rily by innate cells in the lungs, including bronchial epithelial cells (known producers of IL-25), a

197 Immortalized primary bronchial epithelial cell line (BEAS-2B cells), human pr

198 ne expression microarray analysis in a human bronchial epithelial cell line (Beas-2B) stably infected

199 maturation of apical junctions in the human bronchial epithelial cell line 16HBE14o- (16HBE).

200 ARG2 overexpression in a human bronchial epithelial cell line accelerated oxidative bio

201 ion of Stat1 and Stat2 in Vero cells and the bronchial epithelial cell line BEAS-2B.

202 of M. catarrhalis O35E to attach to a human bronchial epithelial cell line in vitro.

203 To test this hypothesis, we used human bronchial epithelial cell line Nuli-1 and C57BL/6 mice.

204 nce the cell viability of human immortalized bronchial epithelial cell line of Beas-2B.

205 C transcript and protein levels in the human bronchial epithelial cell line, 16HBE, Lyn overexpressio

206 nd the growth factor amphiregulin in a human bronchial epithelial cell line.

207 (HBE), and a proliferating, single-cell type bronchial epithelial cell-line (BEAS-2B).

208 The ASL pH of human bronchial epithelial cell lines and primary respiratory

209 ro model using hTERT/Cdk4 immortalized human bronchial epithelial cell lines to identify genes and mi

210 s 40 NSCLC cell lines and do not bind normal bronchial epithelial cell lines.

211 atory variants in the FAM13A region in human bronchial epithelial cell lines.

212 ce and absence of bacterial LPS was shown in bronchial epithelial cells lines (16HBE14o-, CFBE41o-) a

213 basal levels of PINK-1-mediated mitophagy in bronchial epithelial cells, mitochondrial trafficking of

214 of biological liquid bathing a living human bronchial epithelial cell monolayer.

215 nucleotide exchange factors (GEFs) in human bronchial epithelial cell monolayers, we identified GEFs

216 thelial 16HBE cells and primary normal human bronchial epithelial cells (NHBE) at 4-24 h.

217 ust-mite (HDM) induced AAI and primary human bronchial epithelial cells (NHBE) cultured at the air-li

218 ntent of EV secreted by primary normal human bronchial epithelial cells (NHBE) is altered upon asthma

219 Primary normal human bronchial epithelial cells (NHBE) represent a good lung

220 hBE33 cells and normal human bronchial epithelial cells (NHBE) were pretreated with 1

221 nisms and clinical relevance in normal human bronchial epithelial cells (NHBEs) and nasal polyp tissu

222 istobalite silica exposures in primary human bronchial epithelial cells (NHBEs).

223 In primary human bronchial epithelial cells, OA-NO2 blocked phosphorylati

224 PTCH1 mRNA expression was measured in bronchial epithelial cells obtained from individuals wit

225 ole of miRNAs in regulating proliferation of bronchial epithelial cells obtained from severe asthmati

226 ntracytoplasmic inclusion bodies in ciliated bronchial epithelial cells of fatal cases.

227 y glycosylated and shows minimal activity in bronchial epithelial cells of patients with cystic fibro

228 l type producing RNase 7 in cultured primary bronchial epithelial cells (PBEC).

229 We used a combination of primary bronchial epithelial cells (pBECs) from COPD and healthy

230 bronchial epithelial 16HBE cells and primary bronchial epithelial cells (PBECs) from healthy subjects

231 nses were quantified in biopsies and primary bronchial epithelial cells (PBECs) in response to RSV, p

232 es (MDMs), alveolar macrophages, and primary bronchial epithelial cells (PBECs) were isolated from he

233 ial cell line (BEAS-2B cells), human primary bronchial epithelial cells (PBECs), and PBECs derived po

234 reaction to NiV in primary porcine and human bronchial epithelial cells (PBEpC and HBEpC, respectivel

235 In normal human bronchial epithelial cells, pH1N1low-1 was significantly

236 uman microRNA (hsa-miR)-375 in primary human bronchial epithelial cells (pHBEC).

237 that was tested in BEAS-2B and primary human bronchial epithelial cells (pHBECs) using formoterol and

238 SLC26A9 immunofluorescence in primary human bronchial epithelial cells (pHBEs) homozygous for F508de

239 Human bronchial epithelial cells play a key role in airway imm

240 ure to hypoxia led to a profound increase in bronchial epithelial cell proliferation mainly confined

241 Bronchial epithelial cell proliferation was evaluated by

242 ased; these alterations were not observed in bronchial epithelial cells recovered after treatment wit

243 In bronchial epithelial cells recovered from asthmatic vs h

244 nterfering RNA-mediated knockdown of FOXO in bronchial epithelial cells resulted in reduced expressio

245 tistep growth curves in differentiated human bronchial epithelial cells revealed no growth deficiency

246 We sought to enrich for sputum-derived human bronchial epithelial cells (sHBECs) and sputum-derived m

247 Analyses in BEAS-2B immortalized bronchial epithelial cells showed rapid PTP-mediated dep

248 In human primary bronchial epithelial cells ST2 mRNA and protein expressi

249 from air-liquid interface cultures of human bronchial epithelial cells stimulated with IL-6 and sIL-

250 eosinophils migrated toward supernatants of bronchial epithelial cells stimulated with ragweed extra

251 monstrate in cell lines and in primary human bronchial epithelial cells that 3OC12 is rapidly hydroly

252 onfirmed in primary cultures of normal human bronchial epithelial cells that A(2)-isoprostane inhibit

253 e identified potential HHIP targets in human bronchial epithelial cells that may contribute to COPD p

254 erleukin-8 mRNA in BEAS-2B and primary human bronchial epithelial cells through activation of both TR

255 -genome sequence and RNA sequence from human bronchial epithelial cells to dissect functional genes/S

256 Our results show that direct exposure of bronchial epithelial cells to HDM leads to the productio

257 the response of well-differentiated cultured bronchial epithelial cells to interleukin-13 (IL-13).

258 ur data show that in vitro exposure of human bronchial epithelial cells to O3 results in the formatio

259 Exposure of primary human bronchial epithelial cells to wood smoke extract sequent

260 Gene expression of primary bronchial epithelial cells treated with IL-31 was also m

261 dogenous expression of miR-4423 increases as bronchial epithelial cells undergo differentiation into

262 ndividual granules in differentiated primary bronchial epithelial cells using fluorescence lifetime i

263 ure on genome-wide DNA methylation of target bronchial epithelial cells, using 17 volunteers, each ra

264 ls toward supernatants of ragweed-stimulated bronchial epithelial cells was analyzed.

265 nd diesel exhaust particle exposure in human bronchial epithelial cells was associated with altered T

266 adherence to pharynx, type II alveolar, and bronchial epithelial cells was mainly attributed to fibr

267 rent cell lines, well-differentiated primary bronchial epithelial cells (WD-PBECs), and RSV isolates

268 iated primary pediatric nasal (WD-PNECs) and bronchial epithelial cells (WD-PBECs).

269 three-dimensional cultures of primary human bronchial epithelial cells, we demonstrated that loss of

270 e direct DNA-damaging effect of HDM on human bronchial epithelial cells, we exposed BEAS-2B cells to

271 In primary bronchial epithelial cells, we found that basolateral, b

272 Using primary human bronchial epithelial cells, we show that the jamming tra

273 hylation studies in saliva, PBMCs, and human bronchial epithelial cells were done to support our find

274 Human bronchial epithelial cells were exposed to medium alone

275 Correspondingly, human lung fibroblasts and bronchial epithelial cells were found to express DR3 and

276 16HBE14o- bronchial epithelial cells were grown on Transwell inser

277 Normal human bronchial epithelial cells were grown to goblet or norma

278 No cytotoxic effect was observed when bronchial epithelial cells were incubated with PEG-PLGA

279 Transfection studies of bronchial epithelial cells were performed to determine t

280 Primary bronchial epithelial cells were stimulated with IL-17A a

281 tures induced in vitro by IL-17 and IL-13 in bronchial epithelial cells were used to identify patient

282 Human bronchial epithelial cells were used to investigate cyto

283 BEAS2B (bronchial epithelial) cells were treated with IL-4 follo

284 lar epithelial cell lines, and primary human bronchial epithelial cells, were stimulated with LIGHT a

285 ificantly inhibited by mucus in normal human bronchial epithelial cells whereas pH1N1-1 is not.

286 ma-specific miRNA profiles were reported for bronchial epithelial cells, whereas sncRNA expression in

287 ylguanine in nitrosomethylurea-treated human bronchial epithelial cells, while also reducing MGMT pro

288 gene and protein levels, in peptide-treated bronchial epithelial cells with a functional or mutated

289 Treating CF bronchial epithelial cells with a miR-31 mimic decreased

290 However, NY/108 virus replicated in human bronchial epithelial cells with an increased efficiency

291 Stimulation of cultured human bronchial epithelial cells with IL-13, a key mediator in

292 Stimulation of primary bronchial epithelial cells with IL-17A enhanced mRNA exp

293 Transfecting human bronchial epithelial cells with miR-629-3p mimic induced

294 nhalation caused dose-dependent increases in bronchial epithelial cells with puncta of both total ubi

295 Treatment of ZZ primary bronchial epithelial cells with purified plasma M alpha1

296 ull)), TLR4(Hi), and TCM(Hi) cells and human bronchial epithelial cells with small interfering RNA-in

297 d pertussis toxin-sensitive IL-8 response in bronchial epithelial cells, with a higher production of

298 H7N9 viruses replicated efficiently in human bronchial epithelial cells, with subtle changes in pH fu

299 We study here the motion of human bronchial epithelial cells within a monolayer, over long

300 , MX/7218 replicated to high titers in human bronchial epithelial cells, yet it downregulated numerou