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1 ient in the ability to activate NF-kappaB in airway epithelium).
2  shows the receptors are highly expressed in airway epithelium.
3 SM impair barrier function in differentiated airway epithelium.
4 c activity that is capable of disrupting the airway epithelium.
5 Sox2 expression and ultimately generates the airway epithelium.
6 that spores associated with the alveolar and airway epithelium.
7 zed to complementary domains surrounding the airway epithelium.
8 receptors and to alkaline phosphatase in the airway epithelium.
9 ive passage of inhaled allergens through the airway epithelium.
10  such studies have not been reported for the airway epithelium.
11 ) is a major pathogen that primarily infects airway epithelium.
12  to IL-17-mediated downregulation of CRPs on airway epithelium.
13 the apical membrane of surface and glandular airway epithelium.
14 hich to study RSV cytopathogenesis in infant airway epithelium.
15 ain lung structure affected: alveolar versus airway epithelium.
16 st expression of miR-218-5p in the bronchial airway epithelium.
17 M protein levels were increased in asthmatic airway epithelium.
18 secretion of cytokines and chemokines by the airway epithelium.
19 increasing cytokine and LTC(4) generation in airway epithelium.
20 ion of and the subsequent destruction of the airway epithelium.
21 ease of neutrophil proteases that damage the airway epithelium.
22 hat in blood and is tightly regulated by the airway epithelium.
23 , whereas the tracheal cells form a ciliated airway epithelium.
24 omote the goblet cell fate in the developing airway epithelium.
25 ial fibrosis, and increased thickness of the airway epithelium.
26 nterface to reproduce a fully differentiated airway epithelium.
27 ferent severities of asthma for studying the airway epithelium.
28 re PSMCs after naphthalene-induced injury to airway epithelium.
29 ntegrin and were closely associated with the airway epithelium.
30 ressing human SPLUNC1 exclusively within the airway epithelium.
31 ated cell membrane proteins in the polarized airway epithelium.
32 o anti-HPIV activity in cell lines and human airway epithelium.
33 d increases the rate of morphogenesis of the airway epithelium.
34 ally infects the ciliated cells in the human airway epithelium.
35 s normally expressed in gastrointestinal and airway epithelium.
36  cell fate and differentiation events in the airway epithelium.
37 inflammatory responses that could injure the airway epithelium.
38 essed some, but not all, markers of proximal airway epithelium.
39 r very high or very low levels in the normal airway epithelium.
40  and induce mitochondrial dysfunction in the airway epithelium.
41 5AC regulation by IL-1beta and IL-17A in the airway epithelium.
42 phages were restrained by CD200 expressed on airway epithelium.
43 y modulate the expression of lectin genes in airway epithelium.
44 xide released from the apical surface of the airway epithelium.
45 ous Duoxa1 on apical plasma membranes of the airway epithelium.
46 nism of dysregulated iron homeostasis of the airway epithelium.
47 determine the appropriate development of the airway epithelium.
48 helial cells contribute to the repair of the airway epithelium.
49  chloride transport in cystic fibrosis human airway epithelium.
50 teration and preserved the morphology of the airway epithelium.
51  human respiratory virus is delivered to the airway epithelium.
52  cells transfer MeV infectivity to the human airway epithelium.
53 f a subset of progenitor cells in the distal airway epithelium.
54 g mechanism that maintains quiescence in the airway epithelium.
55 on of the virus in polarized human bronchial airway epithelium.
56 derstanding of their interactions with human airway epithelium.
57 act innate antiviral immune responses in the airway epithelium.
58 . aeruginosa adhesion to and invasion of the airway epithelium.
59 insights into RSV interaction with pediatric airway epithelium.
60 hich to characterize its rapid spread in the airway epithelium.
61  of lactate dehydrogenase A occurring in the airway epithelium.
62 PIV-3) infection is highly restricted to the airway epithelium.
63 uring infection of polarized human bronchial airway epithelium.
64 mily member 3), which is highly expressed in airway epithelium.
65 d mature multiciliated cells in a functional airway epithelium.
66 rmal and cystic fibrosis (CF) cultured human airway epithelium.
67 raction of M. pneumoniae with differentiated airway epithelium.
68 geal submucosal glands and in the conducting airway epithelium after pulmonary allergen exposure in v
69 diverse functions ranging from shielding the airway epithelium against pathogenic infection to regula
70                                     In human airway epithelium air-liquid interface (HAE-ALI) culture
71 similar upregulation of IL-33 protein in the airway epithelium, along with marked eosinophilic bronch
72           The deficiency of Splunc1 in mouse airway epithelium also results in increased biofilm form
73          We sought to examine sPLA2-X in the airway epithelium and airway wall of patients with asthm
74 l mice, PSSG was detectable primarily in the airway epithelium and alveolar macrophages.
75 nal gene deletion during the regeneration of airway epithelium and clonal organoid culture.
76  Dual infection induced severe damage to the airway epithelium and confluent pneumonia, similar to th
77 ces IkappaBalpha, an NF-kappaB inhibitor, in airway epithelium and decreases RSV induction of NF-kapp
78 (FcRn), by Calu-3 cell layers simulating the airway epithelium and demonstrates FcRn-mediated cell as
79 d with a loss of the structural integrity of airway epithelium and dysfunction of the physical barrie
80 investigate the effects of IL-17 activity on airway epithelium and identified CXCL5 and MIP-2 as impo
81 1/phosphotyrosine staining patterns in mouse airway epithelium and increased Muc1 tyrosine phosphoryl
82 mplications these results might have for the airway epithelium and its relation to airway inflammatio
83 in expression was significantly increased in airway epithelium and lamina propria of asthmatic patien
84 profiles in prior studies performed on small-airway epithelium and lung parenchyma, suggesting that t
85 rnative NF-kappaB pathways occurs within the airway epithelium and may coordinately contribute to all
86 onal TRPV1 channels are present in the human airway epithelium and overexpressed in the airways of pa
87 tion results in a loss of Nogo expression in airway epithelium and smooth muscle compared with nonall
88 eptor layilin is expressed apically in human airway epithelium and that cells infected with lentiviru
89 an absence of ciliated cells from the entire airway epithelium and the epithelium of the submucosal g
90 hree-dimensional finite element model of the airway epithelium and used it to simulate apical constri
91 d the expression of ERp57 in human asthmatic airway epithelium and used murine models of allergic ast
92 ice expressing or deficient in OGG1 in their airway epithelium and various molecular biological appro
93                    Ear1 was also detected in airway epithelium and was reduced in lungs of mice expos
94  Aspiration of gastric acid commonly injures airway epithelium and, if severe, can lead to respirator
95 ls, which exhibit many features of the human airway epithelium, and colon epithelial cells to serve a
96                Pulmonary macrophages (Mphi), airway epithelium, and dendritic cells (DC) are key cell
97 istry detected SAA was in close proximity to airway epithelium, and in vitro SAA triggered release of
98 g is initiated by apical constriction of the airway epithelium, and not by differential cell prolifer
99 I IFN is the predominant IFN produced by the airway epithelium, and TLR3 is the only TLR that mediate
100 mucosa; proliferation of goblet cells in the airway epithelium; and the production of antigen-specifi
101                   HuR-mediated regulation in airway epithelium appears broader than previously apprec
102  populations, cells of the homeostatic adult airway epithelium are long-lived, and little is known ab
103 small epithelial lesions in pseudostratified airway epithelium are missing.
104  humoral immunity in PGD, and identifies the airway epithelium as a target in PGD.
105 se results identify beta2AR signaling in the airway epithelium as capable of controlling integrated r
106 ied urethane-induced NF-kappaB activation in airway epithelium, as well as type II alveolar epithelia
107                                       In the airway epithelium, basal cells function as stem/progenit
108 fied NLRP3 and caspase-1 expression in human airway epithelium bronchus and primary cells, (2) charac
109 ) lungs, cell proliferation increased in the airway epithelium but apoptosis increased in the blood v
110                         Ablation of Sirt1 in airway epithelium, but not in myeloid cells, aggravated
111  colds, disrupts the barrier function of the airway epithelium by increasing reactive oxygen species
112 r of the airway involves regeneration of the airway epithelium by stem cells in both the proximal air
113                                          The airway epithelium can express factors that drive subepit
114  a reduced chemokine response from polarized airway epithelium cells compared to wild-type strains.
115 ne TGF-beta1 upregulates sialidases in human airway epithelium cells, lung fibroblasts, and immune sy
116 ng activities, and its capacity to stimulate airway epithelium cells.
117         Small wounds in the pseudostratified airway epithelium close within hours to preserve epithel
118 o produce a pseudostratified, differentiated airway epithelium composed of ciliated and nonciliated c
119           Our results demonstrate that human airway epithelium contains a functional NLRP3 inflammaso
120 on airway epithelial cells, we show that the airway epithelium controls a range of pathological respo
121                                              Airway epithelium converts 25-hydroxyvitamin D3 (storage
122 gated whether NF-kappaB pathway signaling in airway epithelium could decisively impact inflammatory p
123 arning about the changes that develop in the airway epithelium could improve our understanding of ast
124 herefore, targeting inflammatory pathways in airway epithelium could prove to be an effective therape
125 asmid and viral infection of polarized human airway epithelium cultured at an air-liquid interface (H
126 ocavirus 1 infects polarized human bronchial airway epithelium cultured at an air-liquid interface th
127 us could be used to deliver CFTR to ciliated airway epithelium derived from CF patients, we inserted
128                                          The airway epithelium develops into a tree-like structure vi
129 lts indicate that miR-4423 is a regulator of airway epithelium differentiation and that the abrogatio
130 to development, postnatal loss of Hdac1/2 in airway epithelium does not affect the expression of Sox2
131  this is comparable to that generated in the airway epithelium during bronchoconstriction in asthma.
132 n were enriched at the apical surface of the airway epithelium during monopodial branching.
133 e upregulation of P2Y4 and P2Y6 receptors in airway epithelium during sensitization.
134  findings suggest that MCMV infection of the airway epithelium enhances goblet cell metaplasia and di
135 or lung epithelial development, in the adult airway epithelium evokes a non-Th2 asthma phenotype that
136                              The superficial airway epithelium exhibits complex regulatory pathways t
137 olecule predominantly expressed in pulmonary airways epithelium, exhibits anti-inflammatory and growt
138 s a field of molecular injury throughout the airway epithelium exposed to cigarette smoke.
139      Thus, persistent NF-kappaB signaling in airway epithelium facilitates carcinogenesis by sculptin
140              Most respiratory viruses target airway epithelium for infection and replication, which i
141                                          The airway epithelium forms a barrier between the internal a
142 nsmokers and 20 healthy smokers and in small airway epithelium from 13 nonsmokers and 20 healthy smok
143                However, IRAK-M expression in airway epithelium from asthmatic patients and its functi
144 ay cilia and effective clearance of the lung airway epithelium from carcinogens.
145 enome miRNA and mRNA expression in bronchial airway epithelium from current and never smokers (n = 20
146 rvey the expression of lectin genes in large airway epithelium from nine nonsmokers and 20 healthy sm
147 viving variant Clara cells (the cells in the airway epithelium from which replacement epithelial cell
148 423 induces a differentiated-like pattern of airway epithelium gene expression and reverses the expre
149 ing a primary culture of mucus-covered human airway epithelium grown at air-liquid interface, without
150  COPD-associated expression in the bronchial airway epithelium had similarly altered expression profi
151             Infection of human cartilaginous airway epithelium (HAE) and a hamster model of disease w
152 ral host cell cultures, a model of the human airway epithelium (HAE) in which primary HAE cells are c
153          An in vitro model of human ciliated airway epithelium (HAE), a useful tool for studying resp
154                             The steady-state airway epithelium has a low rate of stem cell turnover b
155        The functional expression of TRPV1 on airway epithelium has yet to be elucidated.
156                  Studies using ex vivo human airway epithelium have focused on virus tropism, cellula
157 and arginase (ARG), are typical in asthmatic airway epithelium; however, little is known about the me
158 rential expression of microRNA (miRNA) in CF airway epithelium; however, the role of miRNA in regulat
159  To address whether Hsp72 directly activated airway epithelium, human bronchial epithelial cells (16H
160 constitutively active IkappaB kinase beta in airway epithelium (IKTA (IKKbeta trans-activated) mice).
161 quantifies multiple functional parameters of airway epithelium in a colocalized fashion.
162                                          The airway epithelium in alpha7 knockout mice is characteriz
163 electively and effectively inhibit ORMDL3 in airway epithelium in asthma.
164 s that could facilitate investigation of the airway epithelium in future longitudinal pediatric studi
165          IL-22 receptor was localized to the airway epithelium in naive mice but was expressed at the
166 ght to examine mast cell infiltration of the airway epithelium in patients with EIB and the regulatio
167 lted in the persistence of K14+ cells in the airway epithelium in potentially premalignant lesions.
168 etwork that regulates gene expression in the airway epithelium in response to endogenous and exogenou
169 some-mediated IL-1beta production from human airway epithelium in response to PM, and (3) performed i
170 ons of branches within the developing murine airway epithelium in the absence of mesenchyme.
171 aplasia that is composed of cells resembling airway epithelium in the alveolar compartment.
172 differentiation to form the pseudostratified airway epithelium in the developing and adult lung.
173 EC models relative to RSV infection of human airway epithelium in vivo, and future directions for the
174  an authentic surrogate for RSV infection of airway epithelium in vivo.
175 lating many physiological functions of human airway epithelium, including those involving cell morpho
176                     RV-16 infection of human airway epithelium induces glucocorticoid resistance.
177 that selective IL-13 stimulation of Stat6 in airway epithelium induces murine AHR raise questions abo
178  to enhanced fusion and F is a key factor in airway epithelium infection, pathogenesis, and subsequen
179              IFN-gamma signaling through the airway epithelium inhibits eosinophil generation in the
180            IFN-gamma acting only through the airway epithelium inhibits mucus, chitinases, and eosino
181                            Disruption of the airway epithelium is central to many lung diseases, and
182                                          The airway epithelium is comprised of specialized cell types
183                                              Airway epithelium is considered as a major target for lu
184                                    The human airway epithelium is constantly exposed to microbial pro
185 pproaches are feasible, in part, because the airway epithelium is directly accessible by aerosol deli
186       We propose that initial folding of the airway epithelium is driven primarily by apical constric
187                             Integrity of the airway epithelium is essential for normal lung function.
188                                          The airway epithelium is exposed to a range of physical and
189     During pneumococcal pneumonia, the human airway epithelium is exposed to large amounts of H2O2 as
190                                          The airway epithelium is first barrier to interact with, and
191 studies indicate that NF-kappaB signaling in airway epithelium is integral to tumorigenesis in the ur
192 er time, we demonstrate that the human upper airway epithelium is maintained by an equipotent basal p
193  a basolateral protein, and infection of the airway epithelium is not essential for systemic spread a
194  understanding of the regulatory role of the airway epithelium is required to develop new therapeutic
195 ow demonstrate that beta2AR signaling in the airway epithelium is sufficient to mediate key features
196 e, transgenic expression of beta2ARs only in airway epithelium is sufficient to rescue IL-13-induced
197                                          The airway epithelium is the first barrier encountered by re
198                                          The airway epithelium is the first line of defense against i
199                                          The airway epithelium is the first line of host defense agai
200                                              Airway epithelium is the initial point of host-pathogen
201        A characteristic feature of the human airway epithelium is the presence of ciliated cells bear
202                                              Airway epithelium is the primary target of many respirat
203 D smokers (n = 36), with corresponding large airway epithelium (LAE) data included in a subset of sub
204 3(-), a process which is dysfunctional in CF airway epithelium leading to ASL acidification and that
205 munological and physical barrier function of airway epithelium, leading to allergic sensitization, ai
206 ity of this tool by using the example of the airway epithelium lineage.
207 lial function/secretion, suggesting that the airway epithelium may be particularly important in asthm
208 ized that effects of mineral exposure in the airway epithelium may dictate deviating molecular events
209                       Barrier dysfunction of airway epithelium may increase the risk for acquiring se
210 uestering kaiso in the nucleus of a smoker's airway epithelium may represent a novel approach of trea
211 y chemoreceptors offers a means by which the airway epithelium may trigger an epithelial inflammatory
212                                    Bronchial airway epithelium may ultimately serve as a relatively a
213 er-sensing complex, plays a critical role in airway epithelium-mediated immune responses to urban par
214 protein that likely plays a critical role in airway epithelium-mediated innate immune response.
215 ave raised the concern that desialylation of airway epithelium might increase susceptibility to Strep
216 indirect airway hyperresponsiveness, and the airway epithelium might serve as an important regulator
217 ies to inhibit ERp57 specifically within the airways epithelium might provide an opportunity to allev
218 gated in a fully differentiated, mucociliary airway epithelium model.
219       Our results demonstrate that the human airway epithelium mounts virus-specific immune responses
220 d lung microbiome, bacterial invasion of the airway epithelium, NF-kappaB activation, leukocyte infil
221  show that ERp57 levels are increased in the airway epithelium of asthmatic patients and in mice with
222 ecently been shown to be up-regulated in the airway epithelium of asthmatics and to increase active T
223 ork among 5492 genes expressed in human lung airway epithelium of healthy non-smokers, healthy smoker
224  the decreased expression of intelectin 1 in airway epithelium of healthy smokers compared with healt
225 enetic approaches to inactivate STAT3 in the airway epithelium of mice.
226            STUB1 expression was evaluated in airway epithelium of patients with asthma and lung tissu
227    TAK1 phosphorylation was increased in the airway epithelium of patients with fibrotic airway disea
228  along with increased Il33 expression in the airway epithelium of Scnn1b-Tg mice.
229 sfunction induced by deficiency of UQCRC2 in airway epithelium of sensitized BALB/c mice prior the RW
230                                          The airway epithelium of smokers acquires pathological pheno
231 ceptible to pulmonary infection and that the airway epithelium of smokers with chronic obstructive pu
232 tin 1 expression was also decreased in small airway epithelium of smokers with lone emphysema and nor
233 ter methylation in cells exfoliated from the airway epithelium of smokers.
234                         The pseudostratified airway epithelium of the lung contains a balanced propor
235          Branching morphogenesis sculpts the airway epithelium of the lung into a tree-like structure
236                             Pseudostratified airway epithelium of the lung is composed of polarized c
237 pressing an ovalbumin transgene in the small airway epithelium of the lungs (CC10-OVA mice).
238 modeling (TGF-beta1, ADAM8) were detected in airway epithelium of these mice.
239 ional deletion of the Foxm1 gene from either airway epithelium or myeloid inflammatory cells decrease
240 rate mice selectively deficient in ORMDL3 in airway epithelium (Ormdl3(Delta2-3/Delta2-3)/CC10) to si
241 an RT-PCR in both large (p < 0.05) and small airway epithelium (p < 0.02).
242 ls (large airway epithelium, p < 0.01; small airway epithelium, p < 0.01).
243 osyl residues in bacterial cell walls (large airway epithelium, p < 0.01; small airway epithelium, p
244        Expanded cells can produce functional airway epithelium physiologically responsive to clinical
245                               Insults to the airway epithelium play a key role in constrictive bronch
246 rosis transmembrane conductance regulator in airway epithelium plays a critical role in the initial c
247                                          The airway epithelium plays an essential role in innate immu
248                                          The airway epithelium possesses many mechanisms to prevent b
249 sion of a dominant inhibitor of NF-kappaB in airway epithelium prevented lung inflammation and injury
250  transcriptomic alterations in the bronchial airway epithelium reflect molecular events found at more
251 on and antagonism of host responses by human airway epithelium remains poorly understood.
252 se homolog dual oxidase 1 (DUOX1) within the airway epithelium represents a key mechanism of innate a
253 sely, loss of Npy in Foxp1- and Foxp4-mutant airway epithelium rescued the AHR phenotype.
254                  MCMV was able to infect the airway epithelium, resulting in decreased expression of
255                Expression microarrays of the airway epithelium revealed mast cell proteases among the
256                              Analysis of the airway epithelium revealed that EGFR is enriched in airw
257                                    The small airway epithelium (SAE), the first site of smoking-induc
258 e between host and external environment, the airway epithelium serves as a major protective barrier.
259                                           In airway epithelium, SMAD signaling promotes differentiati
260 HDM) leads to robust STAT3 activation in the airway epithelium, smooth muscle, and immune cells in th
261                     Upon colonization of the airway epithelium, specific host cell receptors interact
262 ere we sought to examine the contribution of airway epithelium-specific ERp57 in the pathogenesis of
263                   Recent research shows that airway epithelium stem cells divide mostly asymmetricall
264 posure increased periostin expression in the airway epithelium, subepithelium, smooth muscle and infl
265 rtion of ciliated cells in cultures of human airway epithelium than did viruses with 222D or 222E, wh
266 , these factors act locally on a susceptible airway epithelium that is both structurally and function
267 TSLP) is a cytokine produced by the skin and airway epithelium that is capable of directing dendritic
268 ific gene expression signatures in bronchial airway epithelium that reflect activation of signaling p
269 ing alters expression of TLRs in human small airway epithelium, the primary site of smoking-induced d
270                                   In damaged airway epithelium, they are exposed directly to aeroalle
271            House dust mite (HDM) acts on the airway epithelium to induce airway inflammation in asthm
272  play a critical role in the response of the airway epithelium to injury and are recently recognized
273 ess an activator of the NF-kappaB pathway in airway epithelium to investigate the impact of epithelia
274                       The response of the CF airway epithelium to the opportunistic pathogen Pseudomo
275 the importance of paracrine signals from the airway epithelium to the underlying smooth muscle to ind
276  embryonic tracheal explants and adult human airway epithelium treated with Notch agonists displayed
277 erved in bronchoalveolar lavage macrophages, airway epithelium, vascular endothelium, and airway smoo
278 lays an important role in mucin secretion by airway epithelium via regulation of MARCKS phosphorylati
279 hese data indicate that RSV infection of the airway epithelium, via the action of NS2, promotes epith
280 titative analysis of NF-kappaB activation in airway epithelium was accomplished using a polyclonal an
281 activity in cultured cell lines and in human airway epithelium was assessed by the reduction in viral
282 tion, a conditional knockout of STAT3 in the airway epithelium was generated, e-STAT3-/-.
283                                          The airway epithelium was mostly preserved in syngeneic graf
284 Because the influenza virus is tropic to the airway epithelium, we investigated the role of syndecan-
285 p understand RSV interactions with pediatric airway epithelium, we previously developed three-dimensi
286 terial biofilm formation associated with the airway epithelium, we show that respiratory viral infect
287 boxylase protein in alveolar regions but not airway epithelium; we conclude that tissue specificity l
288 r transgenic mice overexpressing Grx1 in the airway epithelium were analyzed after infection with P.
289 ly active IkappaB kinase beta (CAIKKbeta) in airway epithelium were tolerized to inhaled ovalbumin.
290         TSLP expression was localized to the airway epithelium, whereas IL-33 was expressed in epithe
291 eal rings, an effect that depended on intact airway epithelium, whereas mMCP-4 inhibited IL-13-induce
292  increased levels of eotaxin-1 expression in airway epithelium which was associated with increased nu
293  TLR7 deficiency increased viral load in the airway epithelium, which became sloughed and necrotic, a
294 itative data on the recovery dynamics of the airway epithelium, which can include secretory cell de-d
295                IFN-gamma actions through the airway epithelium will limit airway obstruction and infl
296  sustains arginine availability in asthmatic airway epithelium with consequences for bioenergetics an
297 tides results in peptide accumulation in the airway epithelium with minimal systemic levels of peptid
298 xpression of chemokines such as eotaxin-1 in airway epithelium with resultant recruitment of cells ex
299 ich human PLUNC (hPLUNC) was directed to the airway epithelium with the Scgb1a1 promoter.
300 inflammatory response to viral infections in airway epithelium without jeopardizing viral clearance.

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