ライフサイエンスコーパス: lung epithelial cell

1 terized by the loss and aberrant function of lung epithelial cells.

2 attach to and invade both decidual cells and lung epithelial cells.

3 ycytidylic acid [poly(I:C)] in primary human lung epithelial cells.

4 ertain anti-inflammatory genes in human A549 lung epithelial cells.

5 induces IL-8/CXCL8 expression and release in lung epithelial cells.

6 ells, whereas there were no differences with lung epithelial cells.

7 none of the strains effectively invaded the lung epithelial cells.

8 antitative measurement of cytolysis of human lung epithelial cells.

9 n, and gain- and loss-of-function studies in lung epithelial cells.

10 cherichia coli-induced IL-8 release in human lung epithelial cells.

11 in-driven feed-forward signaling loop in the lung epithelial cells.

12 adation, which increased cytokine release in lung epithelial cells.

13 gradation and increasing cytokine release in lung epithelial cells.

14 p open and active chromatin respectively, in lung epithelial cells.

15 ssential and sufficient for proliferation of lung epithelial cells.

16 n the ESAT-6 induction of IL-8 expression in lung epithelial cells.

17 AT-6 on the regulation of IL-8 expression in lung epithelial cells.

18 and transient expression strategies in human lung epithelial cells.

19 pendium of gene expression profiles of human lung epithelial cells.

20 ishing lung adenocarcinoma cells from normal lung epithelial cells.

21 nduced Fn14 expression when expressed in rat lung epithelial cells.

22 -8 and induces apoptotic cell death in human lung epithelial cells.

23 a A viral infection on ER stress pathways in lung epithelial cells.

24 ulating an anti-viral state in human-derived lung epithelial cells.

25 on in APCs, but had no significant impact in lung epithelial cells.

26 lammation via induced expression of IL-33 by lung epithelial cells.

27 otypic cultures leads to reduced cohesion of lung epithelial cells.

28 5 was selectively knocked out in fetal mouse lung epithelial cells.

29 promote the clonal expansion of premalignant lung epithelial cells.

30 of unrepaired DNA lesions in differentiated lung epithelial cells.

31 reduced stretch-induced CD147 expression on lung epithelial cells.

32 target gene of Smad1 in the developing mouse lung epithelial cells.

33 contain higher PIC levels than untransformed lung epithelial cells.

34 ssion of ligands for inhibitory receptors on lung epithelial cells.

35 p130 in combination with Rb and p53 in adult lung epithelial cells.

36 ty of 8-oxoguanine DNA glycosylase (OGG1) in lung epithelial cells.

37 epression of endogenous Foxp target genes in lung epithelial cells.

38 ing TIMP1 production when expressed in human lung epithelial cells.

39 pled-receptor activation on ATP release from lung epithelial cells.

40 nduced by crocidolite asbestos in A549 human lung epithelial cells.

41 matory genes in murine fibroblasts and human lung epithelial cells.

42 is induction by Fas ligand (FasL) in primary lung epithelial cells.

43 phils, and preventing bacterial adherence to lung epithelial cells.

44 A expression and protein secretion from A549 lung epithelial cells.

45 cytosis, transformation and tumorigenesis of lung epithelial cells.

46 ng adenocarcinomas when compared with normal lung epithelial cells.

47 V-induced lysis of mammalian fibroblasts and lung epithelial cells.

48 ated in allergen-challenged human and murine lung epithelial cells.

49 of human lung carcinoma and CNT-transformed lung epithelial cells.

50 ar lavage fluid (BALF) and culture medium of lung epithelial cells.

51 hibits reactive oxygen species production in lung epithelial cells.

52 ls for normal and oncogene-transformed human lung epithelial cells.

53 ed to catalase, reversed oxidative stress in lung epithelial cells.

54 n enhanced IL-33-induced cytokine release in lung epithelial cells.

55 KRAS-induced transformation of immortalized lung epithelial cells.

56 d gain of function studies were performed in lung epithelial cells.

57 rnalization of Staphylococcus aureus by A549 lung epithelial cells.

58 apoptosis or interferon expression in human lung epithelial cells.

59 th factor beta 1 (TGF-beta1) mediated EMT in lung epithelial cells.

60 cells, but not other NSCLC cells and normal lung epithelial cells.

61 the micro RNA (miRNA) transcriptome in human lung epithelial cells.

62 sion and also attenuated mucus production in lung epithelial cells.

63 nt differentiation into predominantly distal lung epithelial cells.

64 oduction of reactive oxygen species (ROS) in lung epithelial cells (A549 and primary normal human bro

65 ion of diesel exhaust aerosol (DEA) on human lung epithelial cells (A549) in a prototype exposure cha

66 ibution of oxide nanoparticles inside living lung epithelial cells (A549).

67 ne, in mouse lung tissue as well as in human lung epithelial cells (A549).

68 ombin-induced IL-8/CXCL8 expression in human lung epithelial cells (A549).

69 In addition, transfection of ORMDL3 in lung epithelial cells activated ATF6alpha and induced SE

70 MiR-150 conferred a cytoprotective role in lung epithelial cells after oxidative stress, whereas FO

71 uman MG53 (rhMG53) protein protects cultured lung epithelial cells against anoxia/reoxygenation-induc

72 tions of CuO NPs induced IL-8 release in the lung epithelial cells already at subtoxic concentrations

73 erent species (rat and human), two different lung epithelial cells (alveolar type II and bronchial ep

74 affects the expression of selected genes in lung epithelial cells and airway tissue.

75 Intercellular communications between lung epithelial cells and alveolar macrophages play an e

76 lly, miR-155 was also highly expressed in CF lung epithelial cells and circulating CF neutrophils bio

77 into the interaction of this virus with host lung epithelial cells and endothelial cells, which resul

78 ate PcCbk1 after the organism interacts with lung epithelial cells and extracellular matrix component

79 stic fungal pathogen Pneumocystis carinii to lung epithelial cells and extracellular matrix proteins

80 is required for apical junction formation in lung epithelial cells and highlights potential cross-tal

81 rved both in adherence and invasion of human lung epithelial cells and in cytotoxicity of these cells

82 We examined EMT-competent lung epithelial cells and lung fibroblasts from control

83 on of interleukin 8 by wood smoke extract in lung epithelial cells and lung inflammation induced by w

84 tory protein 2 (an interleukin-8 homolog) in lung epithelial cells and lungs and lung inflammation, a

85 ide levels, remarkably, higher expression in lung epithelial cells and macrophages in vitro and in vi

86 important opportunistic fungal pathogen with lung epithelial cells and matrix.

87 d inhibits squamous differentiation in human lung epithelial cells and polymorphisms in human homolog

88 n of the two-pore-domain K channel TREK-1 in lung epithelial cells and proposed a role for this chann

89 ne transfer, MD-2s was strongly expressed in lung epithelial cells and readily detected in bronchoalv

90 cogenic K-Ras is not sufficient to transform lung epithelial cells and requires collaborating signals

91 ted upon S. pneumoniae infection of cultured lung epithelial cells and was critical for AA release fr

92 killing was inducible directly from isolated lung epithelial cells and was not abrogated by the prese

93 that phospho-Akt levels were elevated in CF lung epithelial cells and were specifically lowered by e

94 TC-conjugated dextran through a monolayer of lung epithelial cells, and assessment of bacterial outgr

95 VAMP8 mRNA was present in human airway and lung epithelial cells, and deep-sequencing and expressio

96 sults for primary human keratinocytes, human lung epithelial cells, and murine macrophages.

97 DC-SIGN (SIGN-R1) is present on mouse lung epithelial cells, and SAP and the aminothiazole pot

98 romotes malignant transformation by limiting lung epithelial cell apoptosis and promoting immune esca

99 Here we present evidence that lung epithelial cells are connected by TNTs, and in spit

100 Lung epithelial cells are considered important sources o

101 nesis is a multistep process in which normal lung epithelial cells are converted to cancer cells thro

102 e factor of S. aureus clinical isolates, and lung epithelial cells are highly sensitive to alpha-toxi

103 ed that the majority of EHF binding sites in lung epithelial cells are intergenic or intronic and coi

104 ivator or a repressor, though its targets in lung epithelial cells are largely uncharacterized.

105 PH-dependent redox cycling activity in mouse lung epithelial cells as sepiapterin reductase (SPR), an

106 induced early apoptosis (P < 0.05, n = 6) in lung epithelial cells, as measured by annexin/propidium

107 e expressed in both type I and type II mouse lung epithelial cells, as well as in human lung cancer c

108 croscopy (FM) investigation of exocytosis in lung epithelial cells (ATII cells) allows the detection

109 cal stress on lung fibrotic formation, human lung epithelial cells (BEAS-2B) were exposed to mechanic

110 Although the ST-23 strain attached to lung epithelial cells better than ST-17 and -19 strains,

111 In cultured lung epithelial cells, BMP-4 induced VEGF expression thr

112 that asbestos induces PKD phosphorylation in lung epithelial cells both in vivo and in vitro.

113 increase in interleukin 8 release from A549 lung epithelial cells but decreased interleukin 1beta, i

114 ion is detected in a subpopulation of normal lung epithelial cells, but at very low levels in lung tu

115 nstrated similar levels of adherence to A549 lung epithelial cells, but the mutant strains were defec

116 omonas aeruginosa has the capacity to invade lung epithelial cells by co-opting the intrinsic endocyt

117 the proinflammatory expression of IL-8 in CF lung epithelial cells by lowering SHIP1 expression and t

118 2 expression was induced in rodent and human lung epithelial cells by Th2 cytokines, which was mediat

119 ell, Liu et al. show that TLR3 activation in lung epithelial cells by tumor exosomal RNAs triggers ne

120 Mice in which lung epithelial cells can be induced to express an oncog

121 Lung epithelial cells can influence immune responses to

122 Early-induction of Alk3 knockout in lung epithelial cells caused retardation of early lung b

123 ne genetics to determine how the identity of lung epithelial cells changes upon loss of their master

124 , to the neoplastic-like properties of human lung epithelial cells chronically exposed to a low-dose

125 However, BMP-4 inhibited proliferation of lung epithelial cells, consistent with the increase in p

126 findings suggest that a high viral load from lung epithelial cells coupled with induction of host res

127 demonstrated that autophagy proteins promote lung epithelial cell death, airway dysfunction, and emph

128 FOXD3-AS1 promoted oxidative stress-induced lung epithelial cell death.

129 (LC3B) as a positive regulator of CS-induced lung epithelial cell death.

130 h and thereby exaggerating hyperoxia-induced lung epithelial cell death.

131 been shown to stimulate immune responses in lung epithelial cells, dendritic cells, and alveolar mac

132 erentiated cell cultures, applications using lung epithelial cells derived from ES and iPS cells have

133 We found that lung epithelial cell-derived collagen I activates fibrob

134 ther assess the role of the HIF1a isoform in lung epithelial cell differentiation and homeostasis, we

135 in mesenchyme perturbed trachea development, lung epithelial cell differentiation and lung growth.

136 In human COPD, lung epithelial cells displayed increased expression of

137 than circumference as a large proportion of lung epithelial cells divide parallel to the airway long

138 These findings suggest that cyclic MS of lung epithelial cells down-regulates LPS-mediated inflam

139 scription factor that is highly expressed by lung epithelial cells during development and has been sh

140 s challenge and prevents the injury of human lung epithelial cells during infection.

141 that beta-catenin signaling is activated in lung epithelial cells during neutrophil transmigration,

142 on of the ferric or ferryl HbS with cultured lung epithelial cells (E10) induced a drop in mitochondr

143 HDM and the innate immune response driven by lung epithelial cells (ECs) and dendritic cells (DCs) th

144 In A549 lung epithelial cells, ectopically expressed LtpD locali

145 ltured lung adenocarcinoma but not in normal lung epithelial cells elevated H2S stimulates mitochondr

146 Human lung epithelial cells exposed to hydrogen peroxide (150-

147 Polarized lung epithelial cells express IL-17RA and IL-17RC basola

148 TGF-beta1 secretion is not observed in lung epithelial cells expressing the common SP-A2 varian

149 or potential ankyrin-1 (TRPA1) expression by lung epithelial cells expressing the TRPV1-I585V variant

150 Rat lung epithelial cells expressing v-K-ras or murine lung

151 Apc deficiency altered lung epithelial cell fate by inhibiting Clara and ciliat

152 nterest, expression of Sonic Hh increased in lung epithelial cells following the induction of allergi

153 IP-2 from alveolar macrophages, but not from lung epithelial cells, following 4 h of exposure of cell

154 tes and macrophages (LysM/STAT1) or ciliated lung epithelial cells (FoxJ1/STAT1) deleted were created

155 We show that IFNalpha protects human lung epithelial cells from alpha-toxin-induced intracell

156 so protects Caenorhabditis elegans and human lung epithelial cells from killing by P. aeruginosa.

157 We determined that miR-31 regulates lung epithelial cell growth and identified 6 negative re

158 Additionally, VHR-knockout fibroblast and lung epithelial cells had elevated ligand-induced epider

159 st, transgenic mice that overexpress Grx1 in lung epithelial cells had significantly higher lung bact

160 Injury to lung epithelial cells has a role in multiple lung diseas

161 Lung epithelial cells have emerged as a frequent target

162 WT and usher deletion strains to A549 human lung epithelial cells, HEp-2 human cervical epithelial c

163 cluster is critical for lung development and lung epithelial cell homeostasis and is predicted to tar

164 s essential for buffering Nkx2.1 expression, lung epithelial cell identity, and tissue homeostasis.

165 us of a novel regulatory network, connecting lung epithelial cell identity, migration, and cell-cell

166 Abundantly expressed in lung epithelial cells, IL-33 plays critical roles in bot

167 o-inflammatory cytokines and enzymes in A549 lung epithelial cells in a manner devoid of S1P agonism.

168 55 was more than 5-fold elevated in CF IB3-1 lung epithelial cells in culture, compared with control

169 , and pathogen killing could be induced from lung epithelial cells in isolation.

170 d to transmigrate across monolayers of human lung epithelial cells in the physiological basolateral-t

171 ntified OMVs, which were then used to infect lung epithelial cells in vitro as well as C57BL/6J mice

172 Six1 overexpression in MLE15 lung epithelial cells in vitro inhibited cell differenti

173 In A549 lung epithelial cells in vitro we show that inhibition o

174 Similar findings were observed in human lung epithelial cells in vitro.

175 Loss of Pten in the lung epithelial cells in vivo activated adipokine signal

176 most efficient agent for the transfection of lung epithelial cells in vivo following intra-nasal admi

177 nce that B. anthracis spores are taken up by lung epithelial cells in vivo soon after spores are deli

178 densation and functional delivery of pDNA to lung epithelial cells in vivo.

179 bstantial amounts of spores were taken up by lung epithelial cells in vivo.

180 of human lung and skin fibroblasts, but not lung epithelial cells, in vitro and is present in sclero

181 was specific for tumor compared with normal lung epithelial cells, increased in NSCLCs harvested aft

182 ng to host extracellular matrix proteins and lung epithelial cells induced the phosphorylation (activ

183 nflammation by causing barrier disruption in lung epithelial cells inducing the elevation of interleu

184 s and activated oncogenic signaling in AT II lung epithelial cells, inducing emphysema and adenocarci

185 vivo were compared with those made by human lung epithelial cells infected in vitro with RV16.

186 m on host expression networks by using human lung epithelial cells infected with either wild-type vir

187 Both transformed and primary human lung epithelial cells infected with P. aeruginosa genera

188 Human lung epithelial cells infected with the Le-(U5C, A14G) m

189 ed functional genomics and an in vitro human lung epithelial cell infection model to define the globa

190 Using an in vitro alveolar macrophages and lung epithelial cells infection model, we show significa

191 Compared with wild-type primary lung epithelial cells, infection of Glrx1(-/-) cells wit

192 In conclusion, lung epithelial cells influence the efficacy of most ant

193 siRNA knockdown of ATF-6alpha in lung epithelial cells inhibited expression of SERCA2b, w

194 Lung epithelial cells interconnected by tight junctions

195 We hypothesized that apoptosis of lung epithelial cells is a pathophysiological relevant p

196 Apoptosis of lung epithelial cells is a relevant pathomechanism in th

197 We observed that Pseudomonas invasion of lung epithelial cells is dependent on caveolin-2 but not

198 rleukin-8 induction by wood smoke extract in lung epithelial cells is mediated by novel NADPH oxidase

199 of unrepaired DNA lesions in differentiated lung epithelial cells is unclear.

200 ession of oncogenic K-Ras does not transform lung epithelial cells, it alters the phenotype of the ce

201 In LPS-stimulated A549 human lung epithelial cells, kallistatin attenuated apoptosis,

202 nstrate that water transport across NCI-H441 lung epithelial cell layers and apical surface liquid (A

203 Expression of mutant SP-A2 in lung epithelial cells leads to secretion of latent TGF-b

204 To determine whether IKK2-dependent lung epithelial cell (LEC) responses contribute to the a

205 es the activity of alpha-toxin using a human lung epithelial cell line (A549).

206 croM arsenic treatment for 1-7 days in a rat lung epithelial cell line (L2) using an in-house 10 k ra

207 In a mouse lung epithelial cell line (MLE-15), Nkx2-1 knockdown red

208 5 inhibits SMAD1 and SMAD5 expression in the lung epithelial cell line A549, it inhibits BMP-mediated

209 angement, detachment, and death in the human lung epithelial cell line A549.

210 ng and detachment of cells of the A549 human lung epithelial cell line as well as the Xps-mediated de

211 In the human lung epithelial cell line BEAS-2B, LL-37, but not mCRAMP

212 A lung epithelial cell line, A549, was shown to contain an

213 In a murine lung epithelial cell line, asbestos caused significant i

214 detachment, and death of A549 cells, a human lung epithelial cell line.

215 in RL-65 cells, a spontaneously immortalized lung epithelial cell line.

216 e shown to be cytocompatible with A549 human lung epithelial cell line.

217 In murine lung epithelial cell lines (MLE-15, LA-4) and in primary

218 A similar result was obtained with infected lung epithelial cell lines and the lungs of infected A/J

219 Reduction of Grhl2 in lung epithelial cell lines results in lower expression l

220 synthesizing hepoxilin A(3) are expressed in lung epithelial cell lines, primary small airway epithel

221 nt transforming growth factor (TGF)-beta1 in lung epithelial cell lines.

222 ression in DeltaF508-CFTR and wild type CFTR lung epithelial cell lines.

223 genetic inactivation of KRas(G12D) in mouse lung epithelial cells markedly impairs the progression o

224 w of fetal susceptibility for BPA effects on lung epithelial cell maturation in the third trimester.

225 ng lipid raft-mediated endocytosis to invade lung epithelial cells may depend on the relative strengt

226 cted lungs, suggesting that association with lung epithelial cells may provide an advantage to spore

227 istence of a distinct signaling mechanism in lung epithelial cells mediated by COOH-terminal Src kina

228 Mouse lung epithelial cells (MLE12) transfected with human Mmp

229 Mouse lung epithelial cells (MLE12) with small interfering RNA

230 asing the I-kappaB degradation rate in mouse lung epithelial cells (MLE12).

231 ic surfaces, using a three-dimensional (3-D) lung epithelial cell model.

232 xperimental wound healing in human and mouse lung epithelial cell monolayers and stimulated epithelia

233 hLAL expression in lung epithelial cells not only reduced tumor-promoting m

234 of oncogenic Kras and deletion of p53 in the lung epithelial cells of Kras(LSL-G12D/+);p53(flox/flox)

235 l line (BEAS-2B) and specifically deleted in lung epithelial cells of mice (Stard7(epi/)).

236 To assess how LAL in lung epithelial cells plays a role in this inflammation-

237 Using lung epithelial cells, primary human monocyte-derived ma

238 Lung epithelial cells produce increased hepoxilin A(3) a

239 Factors that affect lung epithelial cell proliferation and activation may be

240 Increases in lung epithelial cell proliferation and bronchoalveolar l

241 d sacculation, accompanied by altered distal lung epithelial cell proliferation and differentiation a

242 RNA knockdown of Suv39H1 or Suv39H2 in fetal lung epithelial cells repressed H3K9 methylation and gre

243 Knockdown of Nur77 in human lung epithelial cells resulted in a marked increase in I

244 Knock-down of FHL2 in human lung epithelial cells resulted in a striking decrease in

245 the CA/09-483HA virus through primary human lung epithelial cells resulted in increased pathogenicit

246 Knockdown of PINK1 expression in lung epithelial cells resulted in mitochondria depolariz

247 KLF6 gene silencing in human lung epithelial cells resulted in the drastic loss of NO

248 reported that IL-8 mRNA is stabilized in CF lung epithelial cells, resulting in concomitant hyperexp

249 itions, C5aR protein was markedly reduced on lung epithelial cells, resulting in much reduced leakage

250 We show that distinct lung epithelial cells secrete acidic mammalian chitinase

251 These studies demonstrate that lung epithelial cells secrete AMCase via an EGFR-depende

252 In the lung, epithelial cells serve as the initial barrier to a

253 Six1(-/-) lung epithelial cells show increased expression of diffe

254 Normal lung epithelial cells show increased rates of migration

255 Eya1(-/-) lung epithelial cells show loss of progenitor cell marke

256 In vitro studies in lung epithelial cells showed that p52 overexpression red

257 ofound effects upon gene expression in human lung epithelial cells, some of which are epigenetically

258 xperimental fibrosis by generating mice with lung epithelial cell-specific loss of alpha3 integrin ex

259 iological effects of K-Ras in nontransformed lung epithelial cells, stable transfectants were generat

260 mitochondrial CYP1B1 was assessed using A549 lung epithelial cells stably expressing shRNA against NA

261 lly, deletion of Smo in Rb1 and Trp53-mutant lung epithelial cells strongly suppressed SCLC initiatio

262 ectin and functional AdipoR1are expressed by lung epithelial cells, suggesting a potential autocrine

263 that induction of ER stress leads to EMT in lung epithelial cells, suggesting possible cross-talk be

264 In human fetal lung epithelial cells, Suv39H1 and Suv39H2 mRNA levels d

265 rge target for microbial invasion, activated lung epithelial cells that are closely apposed to deposi

266 nels expressed by airway sensory neurons and lung epithelial cells that may also be activated by CFA1

267 t that LAL is a critical metabolic enzyme in lung epithelial cells that regulates lung homeostasis, i

268 terferes with the activation of NF-kappaB in lung epithelial cells, the goal of this study was to inv

269 In human lung epithelial cells, the microRNA-150 (miR-150) was id

270 We have previously reported that in mouse lung epithelial cells, the pro-EGF ligands TGFalpha, neu

271 inflammation and canonical Wnt signaling in lung epithelial cells, thereby restricting lung tumorige

272 ernalization with a H2-T6SS mutant) and into lung epithelial cells through a phosphatidylinositol 3-k

273 y the ubiquitin-proteasome pathway in murine lung epithelial cells through lysine 183 as an acceptor

274 duces bacterial adhesion and uptake by human lung epithelial cells, thus protecting M. catarrhalis fr

275 stent Nkx2.1 deficiency and reprogramming of lung epithelial cells to a posterior endoderm fate.

276 tutes a highly pathogenic virus that infects lung epithelial cells to cause a wide spectrum of respir

277 Exposure of human lung epithelial cells to H2O2 induces apoptosis concomit

278 t to investigate the responsiveness of human lung epithelial cells to the TNF family molecules LIGHT

279 A549 lung epithelial cells transfected with plasmid encoding

280 PP2A was silenced in lung epithelial cells treated with A1AT and matrix metal

281 nsing (ECIS) platform to monitor behavior of lung epithelial cells upon exposure to a library of SWCN

282 In accordance, RV16 infection of human lung epithelial cells upregulated TSLP and IL-33 express

283 ression of the leptin/leptin receptor in the lung epithelial cells via activation of MEK/ERK, PI3K/AK

284 independent induction of oxidative stress in lung epithelial cells via the release of bacterial facto

285 an lung cancer, is restrictedly expressed in lung epithelial cells [via Clara cell secretory protein

286 mulator of type II innate lymphoid cells, in lung epithelial cells was associated with suppression of

287 tical region of A549 cells and primary human lung epithelial cells was observed after treatment with

288 Hypoxia-inducible factor-1alpha in lung epithelial cells was shown to regulate interleukin-

289 Using lung epithelial cells, we demonstrate TLR2- and TLR3-tri

290 By using human breast and lung epithelial cells, we have further characterized Del

291 vivo in transgenic mice and human PTEN-null lung epithelial cells, we identify the leptin-driven fee

292 e main pathways through which Na+ ions enter lung epithelial cells, we infected human Clara-like lung

293 Using lung epithelial cells, we show that Alk5-regulated Hes1

294 analyte, air-liquid interface cultured A549 lung epithelial cells were exposed to critical concentra

295 12D) expression occur in a small fraction of lung epithelial cells were generated.

296 Although lung epithelial cells were initially merely regarded as

297 Lung epithelial cells were the main source of CXCL5 upon

298 Rat lung epithelial cells were treated with 52 stimuli, and

299 Therefore, in this study, we irradiated rat lung epithelial cells with different doses of protons an

300 tion induces the early expression of TSLP by lung epithelial cells with multiple consequences.