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1 levels of silencing, particularly in primary airway epithelial cells.
2 induced IL-33 in the induction of CXCL-10 in airway epithelial cells.
3 is study, we deleted the mouse Kif3a gene in airway epithelial cells.
4 s and dendritic cells, transfer infection to airway epithelial cells.
5  given the strict tropism of HBoV1 for human airway epithelial cells.
6 atory effects of R507 were analyzed on human airway epithelial cells.
7 y dependent on IL-33/ST2/IRAK-1 signaling in airway epithelial cells.
8 type-II interferon-gamma (IFNgamma) in human airway epithelial cells.
9 ,3-linked sialic acids on complex glycans on airway epithelial cells.
10 y observed in lung airway using primary lung airway epithelial cells.
11 es but can also inhibit influenza entry into airway epithelial cells.
12 fluenza virus replication in human bronchial airway epithelial cells.
13 ell-differentiated primary cultures of human airway epithelial cells.
14 d release of chemokines, including CCL20, by airway epithelial cells.
15 on TNF-regulated gene expression in cultured airway epithelial cells.
16 d its degradation in the proteasome of human airway epithelial cells.
17 racts with RV RNA and poly(I.C) in polarized airway epithelial cells.
18 ected differentiation of hPSCs into lung and airway epithelial cells.
19 ion are due to infection of nectin4-positive airway epithelial cells.
20 e and regulator of inflammatory signaling in airway epithelial cells.
21 ansepithelial resistance (R(T)) in polarized airway epithelial cells.
22  shedding of the ADAM17 substrate TNFR1 from airway epithelial cells.
23 CFTR by attenuating its endocytosis in human airway epithelial cells.
24 -mediated sodium transport in cultured human airway epithelial cells.
25 vD1 receptors, were expressed on human small airway epithelial cells.
26  various cell types, including primary human airway epithelial cells.
27 ecipitated PP2A in vitro isolated from human airway epithelial cells.
28 10 mRNA, and expression was apparent only in airway epithelial cells.
29 ocrine cells (PNECs) are the only innervated airway epithelial cells.
30 TR and phosphorylates CFTR-Ser(737) in human airway epithelial cells.
31 ibition in both A549 and primary human small airway epithelial cells.
32 ar histones are cytotoxic to endothelial and airway epithelial cells.
33 ly, little to no caspase-1 was detectable in airway epithelial cells.
34 endent CGRP synthesis and secretion by human airway epithelial cells.
35 n led to enhanced binding of conidia to A549 airway epithelial cells.
36 g and release, we examined its expression in airway epithelial cells.
37 compartment or selectively lacking the GR in airway epithelial cells.
38  protein quantification analysis in cultured airway epithelial cells.
39 sing and responding to injured and apoptotic airway epithelial cells.
40 TR loss causes abnormal ion transport across airway epithelial cells.
41 expression, and (3) binding of GR to GREs in airway epithelial cells.
42 own about TGF-beta1 effects on CFTR in human airway epithelial cells.
43 ncreases oxidative and nitrosative stress in airway epithelial cells.
44 odulation following a mechanical stimulus in airway epithelial cells.
45 cocorticoids in regulation of BK channels in airway epithelial cells.
46 g this innate immune response in human small airway epithelial cells.
47 2 in Clara cell secretory protein-expressing airway epithelial cells.
48 rus spreads rapidly and efficiently in human airway epithelial cells.
49 ced CXCL-10 via IRAK-1 depletion at least in airway epithelial cells.
50 s that are infectious in well-differentiated airway epithelial cells.
51  induced expression of both ST2 and IL-33 in airway epithelial cells.
52 ation of beta-catenin to induce EMT in human airway epithelial cells.
53 sm of a discrete population of multiciliated airway epithelial cells.
54 n of noggin, BAMBI, and FSTL1 in human small airway epithelial cells.
55 rity to the transcriptome for intrapulmonary airway epithelial cells.
56 2 strain three times in differentiated swine airway epithelial cells.
57 E shRNA inhibited HMGB1-induced EMT in human airway epithelial cells.
58 EMT-related gene expression in human primary-airway epithelial cells.
59 excessive levels at the apical surface of CF airway epithelial cells.
60 cle DNA with plasmid DNA in transfections of airway epithelial cells.
61 P-regulated ion and fluid transport in human airway epithelial cells.
62 ent them from differentiating into proximal (airway) epithelial cells.
63                           In addition, human airway epithelial cells (16HBE) were challenged with HDM
64 mary rat alveolar epithelial cells and human airway epithelial cells (20-100 microg/cm(2)), primary r
65                            We report that in airway epithelial cells a threshold of p38alpha mitogen-
66  action of extracellularly released HMGB1 in airway epithelial cells (A549 and small airway epithelia
67 separated by a permeable membrane from human airway epithelial cells (A549) infected with RSV with ei
68               Thus, HBoV1 infection of human airway epithelial cells activates antiapoptotic proteins
69  basophil degranulation assays, and in vitro airway epithelial cell activation assays.
70 status in early pregnancy is associated with airway epithelial cell (AEC) responses in new born infan
71                                              Airway epithelial cell (AEC) signaling might regulate HL
72                                              Airway epithelial cells (AEC) are increasingly recognize
73 that air-liquid interface cultures of murine airway epithelial cells (AECs) also actively synthesize
74 estigated TLR expression and polarization in airway epithelial cells (AECs) and the consequences of T
75      Innate immune responses to allergens by airway epithelial cells (AECs) help initiate and propaga
76                                              Airway epithelial cells (AECs) play a critical role in t
77                                              Airway epithelial cells (AECs) provide the first line of
78                                           In airway epithelial cells (AECs), stimulation of PAR2 by a
79 ate and maintain intracellular H2S levels in airway epithelial cells (AECs).
80 of chronic asthma and in vitro human primary airway epithelial cells (AECs).
81                                              Airway epithelial cells also undergo apoptosis after enc
82                                     In human airway epithelial cells, alternative splicing of the IL-
83  of P. aeruginosa grown in sputum gels using airway epithelial cells and a murine infection model.
84 sed expression of inhibitory ligands by both airway epithelial cells and APCs, further establishing a
85        Primary human lung fibroblasts, small airway epithelial cells and blood monocytes were treated
86 genic mice conditionally expressing Foxa3 in airway epithelial cells and developed human bronchial ep
87 ent data has highlighted the cross talk with airway epithelial cells and environmental factors (aller
88  and osmotic stress were assessed in primary airway epithelial cells and ex vivo murine lung tissue.
89              Influenza A virus (IAV) targets airway epithelial cells and exploits the host cell machi
90                    We used the primary human airway epithelial cells and found that the antibodies to
91 l role for p52 in cell survival/apoptosis of airway epithelial cells and implicate noncanonical NF-ka
92  a new role for Rac1-dependent engulfment by airway epithelial cells and in establishing the anti-inf
93 n expression was determined in primary human airway epithelial cells and in mice.
94  expression of pro-inflammatory mediators in airway epithelial cells and in the lung of mice by enhan
95  viruses replicated to higher titre in human airway epithelial cells and in the respiratory tract of
96 as attenuated in two models of primary human airway epithelial cells and in the upper and lower airwa
97 inducible Siglec-F ligand expression by lung airway epithelial cells and inflammatory cells in wild-t
98  element with enhancer activity in 16HBE14o- airway epithelial cells and is enriched for monomethylat
99 human surfactant protein A and annexin A2 on airway epithelial cells and is internalized, leading to
100 ssion in bronchial biopsies was increased in airway epithelial cells and lamina propria inflammatory
101 avage products that acted as TLR4 ligands on airway epithelial cells and macrophages.
102 sociated kinase-1 (IRAK-1) depletion in both airway epithelial cells and macrophages.
103 ge of mammalian cell cultures, human primary airway epithelial cells and mice, but poorly in avian ce
104 s for presentation at the plasma membrane of airway epithelial cells and recognition by CD8(+) T cell
105 on for TREM-1 in neutrophil migration across airway epithelial cells and suggest that it amplifies in
106                 Using in vitro cocultures of airway epithelial cells and T cells and in vivo models o
107  severe asthma and primarily associated with airway epithelial cells and tissue neutrophils.
108 ease inhibitor (SLPI), which is expressed by airway epithelial cells, and IFN-gamma inversely correla
109 lveolar macrophages, monocytes, neutrophils, airway epithelial cells, and in mouse lungs.
110              KCa3.1 was detected in T cells, airway epithelial cells, and myofibroblasts.
111 ctivation was assessed in human neutrophils, airway epithelial cells, and peripheral blood monocytes
112 transcription factor NF-kappaB in conducting airway epithelial cells, and used a combination of in vi
113              Moreover, we show that in human airway epithelial cells AP-2 is not essential for CFTR r
114 ndicating that Runx3 plays a crucial role in airway epithelial cell apoptosis induced by IAV infectio
115 s study, we investigated the hypothesis that airway epithelial cells are a source of CTSS, and mechan
116                                              Airway epithelial cells are the first to encounter aeroa
117                               Although human airway epithelial cells are the main target of respirato
118                                              Airway epithelial cells are the major target for rhinovi
119                                              Airway epithelial cells are the primary targets of RSV i
120 ecule controlling mucus granule secretion by airway epithelial cells as well as directed migration of
121 up-regulated during ciliogenesis in cultured airway epithelial cells, as was DRC2 in C. reinhardtii f
122  multicycle replication in cultures of human airway epithelial cells at 32 degrees C.
123 , was used to monitor EGSH in cultured human airway epithelial cells (BEAS-2B cells) undergoing expos
124  of isoprene SOA on gene expression in human airway epithelial cells (BEAS-2B) through an air-liquid
125 accinia virus (VACV) initially replicates in airway epithelial cells before spreading to secondary si
126 t shown to preserve the barrier integrity of airway epithelial cells better than the human AMP LL-37.
127                         We further show that airway epithelial cells bind chitin in vitro and produce
128                                           In airway epithelial cells, blocking TLR2 enhanced RV-induc
129                 Using cell lines and primary airway epithelial cells (both submerged and well-differe
130 ) luciferase reporter transfected into human airway epithelial cells [both bronchial epithelium + ade
131 ic mucin MUC1 is elevated by inflammation in airway epithelial cells, but the contributions of MUC1 t
132 ductance regulator (CFTR) abundance in human airway epithelial cells by a mechanism that requires ser
133        This study indicates that HBoV1 kills airway epithelial cells by activating genes that suppres
134 und that 25HC inhibits in vitro infection of airway epithelial cells by influenza.
135 atural killer T cells responded to apoptotic airway epithelial cells by secreting cytokines, which me
136  an in vitro model of HRV infection of human airway epithelial cells (Calu-3 cells) and subsequent ex
137 Here we present evidence that differentiated airway epithelial cells can revert into stable and funct
138 inished ENaC-mediated Na(+) absorption in CF airway epithelial cells caused by internalization of a p
139            Air-liquid interface culturing of airway epithelial cells caused widespread changes in miR
140                    Mechanical stimulation of airway epithelial cells causes apical release of ATP, wh
141 dexamethasone to modulate gene expression in airway epithelial cells coincided with its potency to re
142 thylation levels from DNA derived from nasal airway epithelial cells collected from 12 African Americ
143        Activation of NF-kappaB activation in airway epithelial cells correlated with interleukin-8 co
144                                           An airway epithelial cell culture infection model was utili
145 lled direct pH measurements in primary human airway epithelial cell culture models, which also sugges
146  authentic well-differentiated primary human airway epithelial cells cultured at an air-liquid interf
147                                              Airway epithelial cells cultured at an air-liquid interf
148                       Differentiated primary airway epithelial cell cultures (F508del homozygotes) we
149                    Exposure of primary human airway epithelial cell cultures to IFN-gamma for 48 h di
150                             Human and murine airway epithelial cell cultures were also infected with
151 nfant and adult lungs, rhesus monkey primary airway epithelial cell cultures were infected with pande
152                   Intracellular infection of airway epithelial cell cultures with S. aureus led to de
153 tion, and RNA and protein synthesis in human airway epithelial cell cultures, primary lung fibroblast
154 roarray studies using infected primary human airway epithelial cell cultures.
155  composition for dry, direct deposition onto airway epithelial cell cultures.
156 n mice or its inactivation in vitro in human airway epithelial cell cultures.
157 (PLA2G10) expression was examined in primary airway epithelial cell cultures.
158 acking MIWI2 exhibited an altered balance of airway epithelial cells, demonstrating fewer multiciliat
159 reatment-resistant asthma via neutrophil and airway epithelial cell-dependent pathways.
160 m donated blood and (ii) well-differentiated airway epithelial cells derived from donor lungs.
161 initiation of TH 2 responses is regulated by airway epithelial cell-derived factors, including TRAIL
162                        In siRNA-MUC4 BEAS-2B airway epithelial cells dexamethasone produced higher an
163                 Further analysis showed that airway epithelial cells did not produce glucocorticoids
164                   Finally, HMGB1 released by airway epithelial cells due to RSV infection appears to
165 ve Rhizopus and Mucor strains and with human airway epithelial cells during fungal invasion, to revea
166  to potentiate its cytoprotective signals in airway epithelial cells during influenza infection.
167                            Here we show that airway epithelial cells efficiently engulf apoptotic epi
168               RNA was extracted from primary airway epithelial cells either immediately after cell pr
169                       Knockdown of TRIM29 in airway epithelial cells enhances type I interferon produ
170 gulated after allergen challenge, notably in airway epithelial cells, eosinophils, and neutrophils.
171                 Here we report that in human airway epithelial cells Epstein-Barr virus induces TRIM2
172 CTSS activity with the demonstration that CF airway epithelial cells express and secrete significantl
173                                              Airway epithelial cells express arginine-specific ADP ri
174                                        Human airway epithelial cells express pannexin 1 (Panx1) chann
175 suggested that, when approximately 10-50% of airway epithelial cells expressed CFTR, they generated n
176                                    Increased airway epithelial cell expression of CGRP, together with
177 ial cells are committed to the Sox2-positive airway epithelial cell fate, Fgf10 prevents ciliated cel
178                                              Airway epithelial cells form a barrier to the outside wo
179                                  In cultured airway epithelial cells, FP treatment inhibited IL-13-in
180            Consistent with this observation, airway epithelial cells from asthmatic children a produc
181 -148b levels were significantly increased in airway epithelial cells from asthmatic subjects with an
182                            Although isolated airway epithelial cells from Beclin-1(+/-) mice demonstr
183      Studies using pendrin knockout mice and airway epithelial cells from hearing-impaired subjects w
184 t in well-differentiated primary cultures of airway epithelial cells from human donors (HAE), MV infe
185 d to primary cultures of well-differentiated airway epithelial cells from human donors (HAE).
186             The ability to generate lung and airway epithelial cells from human pluripotent stem cell
187  accumulate on the luminal membrane of upper-airway epithelial cells from mice and humans with CF.
188 ell-differentiated primary cultures of human airway epithelial cells from non-CF and CF subjects, tre
189                                  However, in airway epithelial cells from patients with cystic fibros
190  miR-148b, and miR-152) transcript levels in airway epithelial cells from the same subjects.
191                                              Airway epithelial cell gene expression from 155 subjects
192 d a microarray platform to analyze bronchial airway epithelial cell gene expression in relation to th
193                                     Lung and airway epithelial cells generated in vitro from human pl
194  and CCDC65-specific shRNA transduced normal airway epithelial cells had stiff and dyskinetic cilia b
195 ne IL-13 on beta2AR desensitization in human airway epithelial cells (HAECs) and determine whether 15
196 e phosphatase (PTP) activity in single human airway epithelial cells (hAECs) using capillary electrop
197                              Loss of Rac1 in airway epithelial cells has demonstrated its participati
198  that intrinsic developmental differences in airway epithelial cell immune function may contribute to
199  deletion of Rac1 expression specifically in airway epithelial cells in a mouse model resulted in def
200 domain-only protein, Bmf, in human and mouse airway epithelial cells in a p53-dependent manner.
201 s were shown to transform immortalized human airway epithelial cells in a sorafenib-sensitive manner.
202  IL-8 and other proinflammatory mediators by airway epithelial cells in an ALX/FPR2 (formyl peptide r
203 ylation, was up-regulated in mouse and human airway epithelial cells in association with air-space en
204 egulatory mechanisms of ferroptotic death in airway epithelial cells in asthma, kidney epithelial cel
205 we show that expression of SPDEF or FOXA3 in airway epithelial cells in neonatal mice caused goblet c
206  epithelial progenitors into Sox2-expressing airway epithelial cells in part by activating epithelial
207 irway expression, and ATF4 overexpression in airway epithelial cells in vitro recapitulates COPD-asso
208            UA promoted secretion of IL-33 by airway epithelial cells in vitro, and administration of
209 protein either incubated with cultured human airway epithelial cells in vitro, or provided as an aero
210 ir effects on innate interferon responses of airway epithelial cells in vitro.
211 t receptor 1-related protein y expression in airway epithelial cells in vitro.
212 s is associated with NF-kappaB activation in airway epithelial cells in vivo.
213 3(Delta2-3/Delta2-3)/CC10 mice as well as in airway epithelial cells in which ORMDL3 was inhibited wi
214 RNA isolated from primary normal human small airway epithelial cells indicated that IL-17A (100 ng/ml
215 g results showed that RSV infection of human airway epithelial cells induced a significant release of
216 ling, and production of new viral progeny in airway epithelial cells infected with adenovirus type 2.
217 ors find a deficiency in IFN production from airway epithelial cells infected with human rhinovirus i
218    In addition, conditioned media from human airway epithelial cells infected with Pseudomonas aerugi
219 he transcriptional response of primary mouse airway epithelial cells infected with rhinovirus at 33 d
220 canic ash had minimal effect on alveolar and airway epithelial cell integrity.
221                                              Airway epithelial cells interface innate and adaptive im
222 hat stimulation of EGFR activation by ATP in airway epithelial cells is closely associated with dynam
223 ivity of Vero cell-derived virus for primary airway epithelial cells is increased 5-fold if the virus
224 control and IFN response to these viruses in airway epithelial cells is remarkably similar between su
225   However, the role of HMGB1 in EMT of human airway epithelial cells is still unclear.
226 he potential dysregulation of methylation in airway epithelial cells is unknown.
227  observations, deletion of IGF-1 receptor in airway epithelial cells led to exacerbated lung inflamma
228                                        Human airway epithelial cell lines (BEAS-2B and A549) and huma
229                   SPAG1 was present in human airway epithelial cell lysates but was not present in is
230               IL-13 levels were increased in airway epithelial cells, macrophages, type 2 innate lymp
231           When applied directly to polarized airway epithelial cells, mature aCif triggers a reductio
232 ed interferon response to viral infection by airway epithelial cells may be a mechanism leading to lu
233 d, ozone (O3) interacts with cholesterols of airway epithelial cell membranes or the lung-lining flui
234                                              Airway epithelial cells mount a tolerogenic microenviron
235                                     Thus, in airway epithelial cells, MV spread requires the nectin-4
236  A549 cells and were all cytotoxic for small airway epithelial cells, NCI-H441, and normal human lung
237 ted in gene expression profiles of bronchial airway epithelial cells obtained by bronchoscopy.
238 so used to reconstitute ORMDL3 expression in airway epithelial cells of Ormdl3 knockout mice.
239 ed the impact of Hsp27, an sHsp expressed in airway epithelial cells, on the common protein misfoldin
240                     Cultured human or murine airway epithelial cells or mice were subjected to acute
241  to supernatants from IL-1beta-stimulated CF airway epithelial cells (P < .01).
242  Together, these results suggest beta2ARs on airway epithelial cells promote the asthma phenotype and
243                        The results show that airway epithelial cells regulate local immune responses,
244                                   Therefore, airway epithelial cells release less ATP in response to
245 ced, CCR4-dependent release of CGRP by human airway epithelial cells represents a novel inflammatory
246 itivity regions in lung fibroblasts or small airway epithelial cells, respectively.
247                 Many cells, including murine airway epithelial cells, respond to a variety of inflamm
248         However, the molecular mechanisms of airway epithelial cell responses to viral infection are
249               Transfection of caspase-1 into airway epithelial cells restored their ability to secret
250  channel (VDCC)-intervened calcium influx in airway epithelial cells, resulting in a rapid IGF2 secre
251                           Treatment of small airway epithelial cells (SAEC) or lung fibroblasts ex vi
252 nt stem cells (iPSC) from normal human small airway epithelial cells (SAEC) to investigate epigenetic
253 l/tracheal epithelial cells (NHBE) and small airway epithelial cells (SAEC).
254                In normal primary human small airway epithelial cells (SAECs) treated with TGF-beta1 (
255 e physiologically relevant cell lines--small airway epithelial cells (SAECs), macrophages (THP-1 cell
256 nce in both human lung fibroblasts and small airway epithelial cells (SAECs).
257 ucing factor in the RSV-infected human small airway epithelial cell secretome and was differentially
258 pregnancy and aspects of stimulated neonatal airway epithelial cell secretory function that may in tu
259             Th2 cytokine-stimulated cultured airway epithelial cells showed down-regulation of t-PA,
260 wn that influenza virus infection of primary airway epithelial cells strongly enhances PDL-1 expressi
261 nt-resistant membrane fraction prepared from airway epithelial cells, suggesting that it may partitio
262 tophagy is an important adaptive response in airway epithelial cells targeted by many common adenovir
263 gamycin and quercetin is lower in CF-derived airway epithelial cells than in non-CF cells.
264 profound increase in the cytosolic E(GSH) of airway epithelial cells that is indicative of an oxidant
265 eath-receptor-induced programmed necrosis of airway epithelial cells that led to severe bronchiole ep
266 ntrinsic developmental differences in infant airway epithelial cells that may contribute to the incre
267 ed G protein are less infectious for primary airway epithelial cells, the natural RSV target.
268 iR-101 and miR-144 were transfected in human airway epithelial cells, they directly targeted the CFTR
269 we examined the molecular responses of human airway epithelial cells to B. cenocepacia infection.
270  the main risk factor for COPD, and exposing airway epithelial cells to cigarette smoke extract (CSE)
271 l type 2 (Th2) cytokine, transforms cultured airway epithelial cells to goblet cells, and this is not
272 expression is a component of the response of airway epithelial cells to innate immune activation by r
273                         TNF signaled through airway epithelial cells to reprogram them and promote Th
274 and regulating the innate immune response of airway epithelial cells to viral infection.
275 moke and other environmental stimuli acts on airways epithelial cells to induce neutrophil chemotaxin
276 1 in airway epithelial cells (A549 and small airway epithelial cells) to establish its role in RSV in
277  the susceptibility of cells, especially the airway epithelial cells, to hRSV infection.
278 bunit of NF-kappaB, and RNA polymerase II in airway epithelial cells treated with dexamethasone, TNF,
279                                              Airway epithelial cells treated with IL-4 followed by AD
280 protein connexin43 (Cx43) in polarized human airway epithelial cells upon infection by PAO1.
281 le damage to the mitochondria in human small airway epithelial cells, using a precision microbeam irr
282 udied in Chlamydomonas reinhardtii and human airway epithelial cells, using RNA assays and immunostai
283  steroid-resistant inflammatory signature in airway epithelial cells via constitutively expressed LTb
284  to date suggest that these viruses kill the airway epithelial cells via the apoptotic or necrotic pa
285 L17-induced release of CGRP by primary human airway epithelial cells was also observed.
286         ATP-mediated EGFR transactivation in airway epithelial cells was found to involve purinergic
287 x-dependent regulation of EGFR activation in airway epithelial cells was found to strongly depend on
288 sis of Clara cell secretory protein-positive airway epithelial cells was observed in transgenic mice
289          While replication kinetics in human airway epithelial cells was on par with that of seasonal
290  proteins unique to RSV-infected human small airway epithelial cells was regulated by the transcripti
291                          Numbers of necrotic airway epithelial cells were elevated and correlated wit
292 on IFN-gamma treatment, fully differentiated airway epithelial cells were exposed to ammonium chlorid
293                                              Airway epithelial cells, which are the first line of def
294 pressed in mouse taste buds but also in lung airway epithelial cells, which have previously been show
295                                 Infection of airway epithelial cells with RSV led to the production o
296         Here we show that infection of human airway epithelial cells with Streptococcus pneumoniae le
297 o do this, we examined the infection of A549 airway epithelial cells with the live vaccine strain (LV
298 he cells express markers of various lung and airway epithelial cells, with a predominance of cells id
299 y(I:C) to selectively upregulate IFN-beta in airway epithelial cells without a concomitant inflammato
300 s feasible to augment IFN-beta production in airway epithelial cells without excessive costimulation

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