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

1 induced goblet cell differentiation of human bronchial epithelial cells.

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

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

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

5 mouse embryonic fibroblasts and normal human bronchial epithelial cells.

6 replication and impaired TLR3 expression in bronchial epithelial cells.

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

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

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

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

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

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

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

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

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

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

17 internalization of Haemophilus influenzae in bronchial epithelial cells.

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

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

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

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

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

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

24 lls with primary differentiated normal human bronchial epithelial cells.

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

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

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

28 ntified variants was conducted using primary bronchial epithelial cells.

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

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

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

32 cts of IL-13 and corticosteroids on cultured bronchial epithelial cells.

33 lung cancer cell lines than in nonmalignant bronchial epithelial cells.

34 CHRNA5/3 in lung, airway smooth muscle, and bronchial epithelial cells.

35 ted protein kinase signaling to drive EMT in bronchial epithelial cells.

36 d (SULF2U) NSCLC cell lines and normal human bronchial epithelial cells.

37 ession of the corresponding genes in primary bronchial epithelial cells.

38 ary small airway epithelial cells, and human bronchial epithelial cells.

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

40 e whether nickel contributes to EMT in human bronchial epithelial cells.

41 g adenocarcinoma epithelial and normal human bronchial epithelial cells.

42 densate leads to genome instability in human bronchial epithelial cells.

43 onfluent monolayer of polarized normal human bronchial epithelial cells.

44 ing infection of differentiated normal human bronchial epithelial cells.

45 ulation of CHI3L1 expression in normal human bronchial epithelial cells.

46 28 known Rho target proteins in 16HBE human bronchial epithelial cells.

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

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

49 ible activation of oncogenes in immortalized bronchial epithelial cells.

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

51 3O-C12-HSL attenuate PPARgamma expression in bronchial epithelial cells.

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

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

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

55 sulting in malignant transformation of human bronchial epithelial cells.

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

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

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

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

60 otherwise resistant telomerase-immortalized bronchial epithelial cells.

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

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

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

64 he dynamic transcriptional response of human bronchial epithelial cells after infection with influenz

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

66 d PAI-1 immunolabeling in sickle mouse lung, bronchial epithelial cells, alveolar macrophages, and pu

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

68 This loss was most evident in bronchial epithelial cells and associated with an increa

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

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

71 uced IFN-beta and IFN-lambda production from bronchial epithelial cells and IFN-lambda from bronchoal

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

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

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

75 nduced COX-2 expression in both normal human bronchial epithelial cells and mouse embryonic fibroblas

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

77 herence of A. baumannii to both normal human bronchial epithelial cells and normal human neonatal ker

78 or sequences of a type expressed on ciliated bronchial epithelial cells and on epithelia within the l

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

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

81 Bronchial epithelial cells and peripheral blood mononucl

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

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

84 ure of ORMDL3 ER expression in particular in bronchial epithelial cells and suggest an ER UPR pathway

85 d from the conditioned media of normal human bronchial epithelial cells and the bronchoalveolar lavag

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

87 in vitro in HEp-2 cells and in primary human bronchial epithelial cells and were shown to act postent

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

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

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

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

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

93 Bronchial epithelial cells appear to be a more important

94 vivo studies show that mechanically stressed bronchial epithelial cells are a source of secreted TF a

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

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

97 We hypothesized that bronchial epithelial cell (BEC) expression of PD-Ls woul

98 o induce IL-8 and LT production in the human bronchial epithelial cell (BEC) line 16HB14o- was measur

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

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

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

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

103 Bronchial epithelial cells (BECs) produce CC chemokines,

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

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

106 YLKP1 promoter is minimally active in normal bronchial epithelial cells but highly active in lung ade

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

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

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

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

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

112 Unlike results for CF cells, normal bronchial epithelial cells coinfected with MPA/RV showed

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

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

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

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

117 beta mRNA and protein levels was assessed in bronchial epithelial cell cultures.

118 iscosity in both ML and PCL of CF vs. non-CF bronchial epithelial cell cultures.

119 Increased bronchial epithelial cell death was observed as early as

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

121 Human bronchial epithelial cells derived from endobronchial bi

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

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

124 ays and multilayer cultures of primary human bronchial epithelial cells differentiated in an air-liqu

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

126 cretion to approximately 14% of non-CF human bronchial epithelial cells (EC(50), 81 +/- 19 nM), a lev

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

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

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

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

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

132 w show that well differentiated normal human bronchial epithelial cells express CHI3L1 and secrete YK

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

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

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

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

137 Primary human bronchial epithelial cells from asthma patients and cont

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

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

140 Human bronchial epithelial cells from asthmatic volunteers had

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

142 es as well as post-transplant, primary human bronchial epithelial cells from both CF and non-CF patie

143 Human bronchial epithelial cells from healthy and asthmatic su

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

145 Cultured primary bronchial epithelial cells from patients with mild asthm

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

147 Bronchial epithelial cells from the transplanted lung ca

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

149 mmasome and innate immune signaling in human bronchial epithelial cells from volunteers with and with

150 iral replication were compared between human bronchial epithelial cells from volunteers with and with

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

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

153 Normal human bronchial epithelial cells grown in air-liquid interface

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

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

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

157 ncrease oxidative stress and influence human bronchial epithelial cell (HBEC)-dendritic cell interact

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

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

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

161 that a 4-week exposure of immortalized human bronchial epithelial cells (HBEC) to tobacco carcinogens

162 ial cells and cdk-4/hTERT-immortalized human bronchial epithelial cells (HBEC) were cultured in norma

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

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

165 levels of SRC-3 than did immortalized human bronchial epithelial cells (HBEC), which in turn express

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

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

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

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

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

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

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

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

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

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

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

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

178 e compared by infecting human differentiated bronchial epithelial cells in air-liquid interface cultu

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

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

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

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

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

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

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

186 of fully differentiated primary normal human bronchial epithelial cells induces apical and basolatera

187 ed RSV showed that treatment of normal human bronchial epithelial cells induces apical IL-8, IP-10, a

188 erved in normal HFFs but not in normal human bronchial epithelial cells infected by this mutant.

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

190 Ca(2+) agonists in primary cultures of human bronchial epithelial cells is mediated by CFTR by a mech

191 is, the role of nickel in the EMT process in bronchial epithelial cells is not clear.

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

193 In cultured human bronchial epithelial cells isolated from patients with C

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

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

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

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

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

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

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

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

202 we analyzed the proteome response of a human bronchial epithelial cell line to Aspergillus infection

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

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

205 KIAA0907, in 10 NSCLC cell lines and a human bronchial epithelial cell line.

206 e 36 known Cdc42 target proteins, in a human bronchial epithelial cell line.

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

208 The bronchial epithelial cell lines IB3-1 (CF, high UCH-L1 e

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

210 DNA double-strand break assays using human bronchial epithelial cell lines treated with cigarette s

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

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

213 iratory tract, we employed a polarized human bronchial epithelial cell model and primary human monocy

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 cross the entire genome in both normal human bronchial epithelial cells (NHBE) and NHBE cells exposed

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

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

219 Normal human bronchial epithelial cells (NHBE) grown at the air-liqui

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

221 otent stromal cells (hMSCs) and normal human bronchial epithelial cells (NHBEs) and observed the form

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

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

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

225 Cultured primary bronchial epithelial cells of asthmatics had lower caveo

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

227 Their expression appears diminished in bronchial epithelial cells of rhinovirus-infected asthma

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

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

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

234 Bronchial epithelial cell proliferation was evaluated by

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

236 In bronchial epithelial cells recovered from asthmatic vs h

237 and shedding of the 34-kDa sTNFR1 from human bronchial epithelial cells represents a novel mechanism

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

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

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

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

242 Finally, in human bronchial epithelial cells, silencing endogenous STX6 le

243 In primary human bronchial epithelial cells stimulated with periostin and

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

245 ell differentiated primary cultures of human bronchial epithelial cells subjected to hypotonic challe

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

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

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

249 In human respiratory bronchial epithelial cells, this nanoplex activated the

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

251 By establishing transformed bronchial epithelial cells through chronic low-dose arse

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

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

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

255 infection on the innate immune responses of bronchial epithelial cells to rhinovirus (RV) infection.

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

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

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

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

260 uptake in primary well differentiated human bronchial epithelial cells was accompanied by RhoA activ

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

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

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

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

265 sed on well-differentiated primary pediatric bronchial epithelial cells (WD-PBECs), the primary targe

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

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

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

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

270 quired for the collective migration of human bronchial epithelial cells, we identified myosin-IXA (ge

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

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

273 Primary ciliated bronchial epithelial cells were exposed to 5% cigarette

274 Human bronchial epithelial cells were exposed to medium alone

275 the virulence of Pseudomonas, primary human bronchial epithelial cells were exposed to P. aeruginosa

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 Human bronchial epithelial cells were used to investigate cyto

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

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

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

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

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

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

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

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

290 Treating cultured bronchial epithelial cells with IL-17 plus T(H)2 cytokin

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

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

293 Treatment of bronchial epithelial cells with POPG significantly inhib

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