ライフサイエンスコーパス: airway epithelia

1 response to P. aeruginosa by cystic fibrosis airway epithelia.

2 Na(+) conductances were altered in human CF airway epithelia.

3 rain into pannexin 1-mediated ATP release in airway epithelia.

4 n disrupts the barrier function of polarized airway epithelia.

5 retion in normal compared to cystic fibrosis airway epithelia.

6 is transmembrane regulator (CFTR)-expressing airway epithelia.

7 regulation of transcellular ion transport in airway epithelia.

8 r 1 (TfR1), are expressed in polarized human airway epithelia.

9 efects in a fraction of cilia covering mouse airway epithelia.

10 rrent in H441 epithelia and in human primary airway epithelia.

11 ither basolateral or apical interaction with airway epithelia.

12 mal tidal breathing, regulates ASL volume in airway epithelia.

13 elimination from the apical surface of human airway epithelia.

14 rimary cultures of well-differentiated human airway epithelia.

15 stored transepithelial Cl(-) transport to CF airway epithelia.

16 ADA1 (not ADA2) mRNA was detected in human airway epithelia.

17 adenosine regulate mucociliary clearance in airway epithelia.

18 r (CFTR) channel activity in patient-derived airway epithelia.

19 d biofilms on the apical surface of cultured airway epithelia.

20 vector, AAV2/9, across murine nasal and lung airway epithelia.

21 al than the basolateral surface of polarized airway epithelia.

22 rs to efficiently and persistently transduce airway epithelia.

23 ion proteins could prove to be less toxic to airway epithelia.

24 and non-ciliated epithelial cells and mouse airway epithelia.

25 2)-R-dependent Ca(2+)(i) signals in CF human airway epithelia.

26 m to the apical surface of differentiated CF airway epithelia.

27 try into polarized primary cultures of human airway epithelia.

28 ell-differentiated cultures of primary human airway epithelia.

29 arly modulate tight junction permeability in airway epithelia.

30 e increased in CF compared with normal human airway epithelia.

31 e role of NADPH oxidase in H(+) secretion by airway epithelia.

32 demonstration of regulated ATP release from airway epithelia.

33 s underlie cAMP-regulated Na(+) transport in airway epithelia.

34 res of human cystic fibrosis (CF) and non-CF airway epithelia.

35 ithelial cells and well differentiated human airway epithelia.

36 D was identified as the major PDE species in airway epithelia.

37 possess the capacity of differentiating into airway epithelia.

38 absolutely required for apical expression in airway epithelia.

39 lycoprotein-pseudotyped FIV-based vectors in airway epithelia.

40 in the transitional zone of motile cilia in airway epithelia.

41 tors following apical infection of polarized airway epithelia.

42 of adenosine on the mucosal surface of human airway epithelia.

43 esponse to bacterial components in the human airway epithelia.

44 ctors that demonstrate increased tropism for airway epithelia.

45 AV-2/5 and rAAV-2 from the apical surface of airway epithelia.

46 ith vectors applied to the apical surface of airway epithelia.

47 ha was observed in primary cultures of human airway epithelia.

48 plays a role in the expression of RANTES in airway epithelia.

49 ms that resolve these changes to form normal airway epithelia.

50 d them in well-differentiated cultures of CF airway epithelia.

51 d by in situ hybridization, are expressed in airway epithelia.

52 rimary cultures of well-differentiated human airway epithelia.

53 ding and entry through the apical surface of airway epithelia.

54 teases that serve similar functions in human airway epithelia.

55 ateral membrane of well differentiated human airway epithelia.

56 N) localized mainly to the apical surface of airway epithelia.

57 cused on correcting electrolyte transport in airway epithelia.

58 elivering genes and other pharmaceuticals to airway epithelia.

59 most important barriers to gene transfer in airway epithelia.

60 tigated as a vector to transfer CFTR cDNA to airway epithelia.

61 for the osmotic water permeability (P(f)) of airway epithelia.

62 ECs, which differentiate in situ within lung airway epithelia.

63 binding and endocytosis of vectors by human airway epithelia.

64 clinical specimens using reconstituted human airway epithelia.

65 cy of other AAV serotypes at infecting human airway epithelia.

66 derived cytokines on the function of CD40 in airway epithelia.

67 ndoparvovirus, AAV2, in differentiated human airway epithelia.

68 1 to establish persistent infection of human airway epithelia.

69 ted from newborn piglets and ASL on cultured airway epithelia.

70 nd electrolyte transport assays in polarized airway epithelia.

71 nd normal human lung tissue localized DSP to airway epithelia.

72 in primary cultures of human cystic fibrosis airway epithelia.

73 R-dependent anion secretion in primary human airway epithelia.

74 membrane conductance regulator gene to human airway epithelia.

75 e highly efficient in gene delivery to human airway epithelia.

76 mportant for normal CFTR channel function in airway epithelia.

77 MV infection in primary cultures of porcine airway epithelia.

78 2+) release from the ER, and apoptosis in CF airway epithelia.

79 unction in well differentiated primary human airway epithelia.

80 similar paracellular permeabilities in human airway epithelia.

81 y of this potent neutralizer directly to the airway epithelia.

82 sed at the apical membrane of intestinal and airway epithelia.

83 d Klebsiella pneumoniae biofilm formation on airway epithelia.

84 d fluid absorption across colon, kidney, and airway epithelia.

85 various cell types and by stretch/strain in airway epithelia.

86 restored Cl(-) transport to cystic fibrosis airway epithelia.

87 rom asthmatic patients versus that in normal airway epithelia.

88 ic strategy to reduce the inflammation of CF airway epithelia.

89 hloride currents in both CF human and ferret airway epithelia.

90 lls as well as human and ferret CF polarized airway epithelia.

91 an (rich in 2,3N-linked sialic acid) and pig airway epithelia (2,6N-linked sialic acid), significantl

92 In cystic fibrosis airway epithelia, a hyperactivated epithelial Na(+) cond

93 In airway epithelia, a P2XR-mediated Ca(2+) signal may have

94 Airway epithelia absorb Na+ through the epithelial Na+ c

95 rmacologic disruption of barrier function in airway epithelia allowed responses to apical application

96 cantly reduced transepithelial resistance in airway epithelia and altered tight junction permeability

97 cted in cell culture (A549 and primary human airway epithelia and alveolar macrophages) using chemica

98 sed primary cultures of differentiated human airway epithelia and assessed expression of claudins, th

99 ptional response across all subjects in both airway epithelia and BAL cells, with strong association

100 ological processes such as the secretions of airway epithelia and exocrine glands, the contraction of

101 complexes that may degrade DeltaF508-CFTR in airway epithelia and identifies a new role for NEDD8 in

102 rease channel activity in excised patches of airway epithelia and in intact mouse jejunum.

103 ery that is advantageous for growth in human airway epithelia and in vivo confers susceptibility to p

104 n vitro human cystic fibrosis (CF) polarized airway epithelia and in vivo human CF bronchial xenograf

105 R regulates multiciliogenesis in both murine airway epithelia and in Xenopus laevis epidermis.

106 allergic asthma, transcriptional changes in airway epithelia and inflammatory cells are influenced b

107 Airway epithelia and inflammatory cells were obtained vi

108 iates ATP release from hypotonically swollen airway epithelia and investigated mechanisms regulating

109 n the lung, HBD-2 is an inducible product of airway epithelia and may play a role in innate mucosal d

110 ined on the apical surfaces of human and rat airway epithelia and on cow tracheal explants.

111 the potentially deleterious effects of CS on airway epithelia and outline a hitherto unrecognized sig

112 A subunits localize to the apical surface of airway epithelia and PP2A phosphatase activity co-purifi

113 cs that enables on-chip engineering of human airway epithelia and precise reproduction of physiologic

114 opulation of smooth muscle cells surrounding airway epithelia and promote airway differentiation of e

115 nterferon gamma (IFN-gamma), and IL-1beta in airway epithelia and secretions from cystic fibrosis (CF

116 jor adrenergic receptor isoform expressed in airway epithelia and that it colocalizes with CFTR at th

117 to mediate effective gene transfer to human airway epithelia and that the cytoplasmic domain of CAR

118 n complement the CF defect in differentiated airway epithelia and thereby further the development of

119 f elastin fibers seen in normal lung between airway epithelia and underlying smooth muscle cells was

120 CFTR reciprocally regulates AMPK function in airway epithelia and whether such regulation is involved

121 (AQP1) in microvascular endothelia, AQP4 in airway epithelia, and AQP5 at the apical plasma membrane

122 found that BBS genes were expressed in human airway epithelia, and BBS2 and BBS4 localized to cellula

123 f CD103 (Itgae), were mislocalized away from airway epithelia, and demonstrated an impaired ability t

124 failure of vectors to attach and enter into airway epithelia, and may require redirecting vectors to

125 uction in airway cell lines, polarized human airway epithelia, and mouse lungs.

126 ompetitively inhibited bacterial adhesion to airway epithelia, and MUC1-ED immunodepletion completely

127 ional cellular complex with AMPK and CFTR in airway epithelia, and NDPK-A catalytic function is requi

128 of sodium absorption is a function of human airway epithelia, and prostasin is a likely candidate fo

129 nscellular pathway for Cl and HCO in porcine airway epithelia, and reduced anion permeability may ini

130 an important determinant of CFTR activity in airway epithelia, and support the use of PDE4 inhibitors

131 nd mediate gene transfer to human and murine airway epithelia, and the tropism of AAV5 may be useful

132 pH were identified in the apical membrane of airway epithelia, and their activities were measured.

133 bility in non-cystic fibrosis (non-CF) or CF airway epithelia, AQP-transfected Fisher rat thyroid cel

134 at, when polarized/well-differentiated human airway epithelia are infected with HBoV1 in vitro, they

135 Airway epithelia are known to produce inflammatory media

136 The airway epithelia are lined with fluid called airway surf

137 Airway epithelia are positioned at the interface between

138 Earlier work has shown that human airway epithelia are resistant to infection by adenoviru

139 e apical surface of the differentiated human airway epithelia as well as in human tracheal tissue sec

140 predominant basolateral location in cultured airway epithelia as well as in normal human airway tissu

141 lay a critical role in retinol metabolism in airway epithelia as well as in other epithelia of colon,

142 ory coronavirus NL63, was expressed in human airway epithelia as well as lung parenchyma.

143 In human airway epithelia, as well as in transfected Madin-Darby

144 st study investigating the effect of AMPs on airway-epithelia associated genes upon administration to

145 AAV2.5T binds to the apical surface of human airway epithelia at higher levels and has more receptors

146 sed Cl(-) transport in differentiated non-CF airway epithelia but not in CF epithelia.

147 producing isotonic volume responses in human airway epithelia but were typically short acting and les

148 CFTR is expressed in airway epithelia, but how CF alters electrolyte transpor

149 o the apical surface of differentiated human airway epithelia, but only AAV5 infects.

150 and ASL volume homeostasis in non-CF and CF airway epithelia by attenuating Ca(2+) influx.

151 and ASL volume homeostasis in non-CF and CF airway epithelia by attenuating Ca2+ influx.

152 n from the apical surface of human polarized airway epithelia by modulating the intracellular traffic

153 The results indicate that infection of human airway epithelia by SARS coronavirus correlates with the

154 the first time that virus infection of human airway epithelia can also induce pyroptosis.

155 a predominant gel-forming mucin secreted by airway epithelia, can be induced by various inflammatory

156 moter-LUC was transfected into primary human airway epithelia cells (EC), the luciferase activity was

157 In multiple cell lines, including airway epithelia, CFTR diffused little in the plasma mem

158 from the basolateral side of differentiated airway epithelia composed of Calu-3 cells.

159 ) are relatively high for both normal and CF airway epithelia, consistent with an isosmotic ASL.

160 Human airway epithelia constitutively produce both a ligand, t

161 Thus, airway epithelia contain a cell-autonomous system in whi

162 in contrast to AAV2, the apical membrane of airway epithelia contains abundant high affinity recepto

163 Airway epithelia control the pH of airway surface liquid

164 ane conductance regulator to cystic fibrosis airway epithelia, correcting the Cl(-) transport defect.

165 rate that AAV1 transduction biology in human airway epithelia differs from that of AAV2 and AAV5 by v

166 ally or basolaterally to primary cultures of airway epithelia, discrete foci of eGFP expression appea

167 When expressed in well differentiated CF airway epithelia, each construct localized predominantly

168 -adjacent and tumor-distant normal-appearing airway epithelia exhibit somatic driver alterations that

169 These data indicate that the TJ of airway epithelia exposed to chronic inflammation may exh

170 data indicate for the first time that human airway epithelia express catalytically active NEU1 siali

171 part by sialidase activity, we asked whether airway epithelia express catalytically active sialidase(

172 These same airway epithelia express receptors that respond to dange

173 Airway epithelia express sialylated receptors that recog

174 Here we show that the apical membrane of airway epithelia express the urokinase plasminogen activ

175 We found that polarized human airway epithelia expressed abundant FR alpha on their ap

176 Like many other tissues, airway epithelia expressed multiple claudins.

177 In bronchial airway epithelia, extracellular ATP-mediated, apical inc

178 We found that following infection, human airway epithelia first released adenovirus to the basola

179 te surface proteins for migrating across the airway epithelia for Ag and pathogen capture, transport,

180 ctively used to augment rAAV transduction in airway epithelia for gene therapy of cystic fibrosis.

181 We detected alterations in airway epithelia from 22 patients, with an increased fre

182 imilar differences were observed in cultured airway epithelia from CF and non-CF pigs exposed to the

183 ER density was morphometrically analyzed in airway epithelia from normal subjects, DeltaF508 homozyg

184 ntibacterial activity in primary cultures of airway epithelia from people with cystic fibrosis caused

185 creased airway surface liquid pH in cultured airway epithelia from people with cystic fibrosis.

186 t explain their altered ability to transduce airway epithelia from the apical membrane, we examined t

187 d viruses (AAVs) such as AAV5 that transduce airway epithelia from the apical surface are attractive

188 to be inherently ineffective at transducing airway epithelia from the apical surface.

189 Thus, HCoV-229E preferentially infects human airway epithelia from the apical surface.

190 However, AAV serotype 5 infects human airway epithelia from the lumenal surface.

191 In airway epithelia, GPI-CAR localized specifically to the

192 olayers but failed to migrate across primary airway epithelia grown at the air-liquid interface.

193 ivity in an in vitro model of human ciliated airway epithelia (HAE) derived from nasal and tracheobro

194 at infects well-differentiated primary human airway epithelia (HAE) in vitro In human embryonic kidne

195 apical surface of well-differentiated human airway epithelia (HAE).

196 e pathway for virus entry in polarized human airway epithelia has not been investigated.

197 ssing CFTR and increased Na(+) absorption in airway epithelia has remained elusive, although substant

198 t how CF alters electrolyte transport across airway epithelia has remained uncertain.

199 cellular proliferation and differentiation, airway epithelia have a low rate of cell division.

200 We conclude that (a) normal and CF airway epithelia have relatively high water permeabiliti

201 Airway epithelia have various mechanisms that resolve th

202 Here we show that in differentiated human airway epithelia, heregulin-alpha is present exclusively

203 In an in vivo model of DeltaF508 CF airway epithelia, human CF bronchial xenografts infected

204 ilized Ca(2+)(i), which were investigated in airway epithelia in a long term culture in the absence o

205 important for ciliogenesis in multiciliated airway epithelia in mice, and antagonizes canonical Wnt

206 oblet cell metaplasia in nasal and pulmonary airway epithelia in rats.

207 intestine, gallbladder, urinary bladder, and airway epithelia in various animals.

208 ponse profile of IL-13-exposed primary human airway epithelia in vitro and asthmatic airway epithelia

209 lso had no adverse effects on cultured human airway epithelia in vitro.

210 ASL salt concentration in both CF and non-CF airway epithelia in vitro.

211 uman airway epithelia in vitro and asthmatic airway epithelia in vivo.

212 We found that differentiated human airway epithelia inactivated 3OC12-HSL.

213 In air-exposed airway epithelia, induction of factors required for mult

214 This is the first report of pyroptosis in airway epithelia infected by a respiratory virus.IMPORTA

215 ell-differentiated primary cultures of human airway epithelia, infection primarily occurred from the

216 w report, however, that differentiated human airway epithelia internalize rAAV type-2 virus efficient

217 We also found that human airway epithelia internalized significantly more AAV2.5T

218 elicited by apical P2Y(2)-R activation in CF airway epithelia is an expansion of the apical ER Ca(2+)

219 dy shows that adenosine elimination on human airway epithelia is mediated by ADA1, CNT2, and CNT3, wh

220 Antigen exposure via airway epithelia is often associated with a failure to p

221 k has shown that the apical surface of human airway epithelia is resistant to infection by AAV2, pres

222 ltured cells show that the apical surface of airway epithelia is resistant to transduction by AAV2 ve

223 ured CFTR(-/-) and CFTR(DeltaF508/DeltaF508) airway epithelia lacked anion conductance, and they did

224 by fiberoptic bronchoscopy of trachea, large airway epithelia (LAE), and small airway epithelia (SAE)

225 GDS in mast cells, present in stroma of both airway epithelia, lung as well as in other organs.

226 Their expression in airway epithelia may be constitutive or inducible by bac

227 targeting apical receptors in differentiated airway epithelia may be sufficient for gene transfer in

228 Airway epithelia may initiate and amplify inflammation i

229 revious reports suggest that cystic fibrosis airway epithelia may respond to injury by increasing pro

230 This suggests that the airway epithelia might contribute to sensing of H. influ

231 nhibitable aquaporin (AQP) water channels in airway epithelia modulate airway surface liquid volume.

232 NL airway epithelia more rapidly and effectively alkalinize

233 mples] and 80.0 +/- 3.5 [n = 6 samples]) and airway epithelia (mV, mean +/- SEM CFTR-mediated Cl(-) c

234 stitutively expressed at a high level in the airway epithelia of all mammals.

235 omatically acquired molecular alterations in airway epithelia of lung cancer patients has remained un

236 yk expression increased significantly in the airway epithelia of OVA-sensitized and OVA-challenged (O

237 Cas12a RNP achieves editing of loxP sites in airway epithelia of ROSA(mT/mG) mice.

238 In this study, we uncovered that the airway epithelia of these mice also express high levels

239 secreted protein, naturally produced by the airway epithelia of virtually all mammals.

240 While virus-infected airway epithelia often activate NLRP3 inflammasomes, stu

241 d the contribution of the nervous system and airway epithelia on HTS-stimulated ASL height increase i

242 tissues, while no expression was observed in airway epithelia or lung.

243 ltured cystic fibrosis (DeltaF508/DeltaF508) airway epithelia partially restored DeltaF508-cystic fib

244 Virus antigen was observed in airway epithelia, pneumocytes, and macrophages.

245 tic) culture conditions revealed that normal airway epithelia possess an adenosine-regulated pathway

246 E2 exposure inhibited STIM1 translocation in airway epithelia, preventing SOCE.

247 th increased lipopolysaccharide (LPS)-driven airway epithelia production of CXCL1, but not CXCL2, fin

248 This transduction profile in human airway epithelia (rAAV2/1 >> rAAV2/2 = rAAV2/5) was sign

249 In BEAS-2B cells and primary airway epithelia, roflumilast interacted with formoterol

250 hea, large airway epithelia (LAE), and small airway epithelia (SAE) of nonsmokers and smokers were an

251 ACE2 in the human airway epithelium.Methods: Airway epithelia sampled by fiberoptic bronchoscopy of t

252 ncreased in IPF lung and concentrated in the airway epithelia, suggesting a potential role for DSP in

253 ectively processed to the apical membrane of airway epithelia than human DeltaF508-CFTR.

254 a higher binding affinity to the surface of airway epithelia than its parent AAV5.

255 inked sialic acid residues on the surface of airway epithelia that mediate rapid internalization and

256 cultures of normal and cystic fibrosis (CF) airway epithelia that, like the native tissue, contain c

257 In normal airway epithelia, the CCS-induced increase in ASL ATP co

258 In well-differentiated human airway epithelia, the coxsackie B and adenovirus type 2

259 raction between the virus and differentiated airway epithelia; the virus preferentially enters the ce

260 In polarized airway epithelia, this response has been attributed to I

261 me height in normal and cystic fibrosis (CF) airway epithelia through extracellular ATP- and adenosin

262 m cells maintain secretory daughter cells in airway epithelia through forward regulation, suggesting

263 ay also stimulate active secretion of ASL by airway epithelia through the activation of sensory neuro

264 tions, ranging from electrolyte secretion in airway epithelia to cellular excitability in sensory neu

265 previously used directed evolution in human airway epithelia to create adeno-associated virus 2.5T (

266 These data suggest that the ability of human airway epithelia to inactivate quorum-sensing signal mol

267 We investigated the ability of non-CF and CF airway epithelia to kill bacteria through the generation

268 fect this pathway by reducing the ability of airway epithelia to respond appropriately to nucleotides

269 and pro-inflammatory chemokine responses of airway epithelia to rhinovirus and viral mimics and decr

270 Exposure of 30-40-day-old cultures of normal airway epithelia to supernatant from mucopurulent materi

271 nt deleting residues 708-759 complemented CF airway epithelia to the same extent as wild-type CFTR an

272 By contrast, the response of airway epithelia to the stimuli presented by mucoid P. a

273 The adult lung is largely quiescent, with airway epithelia turning over slowly.

274 y of NTHi to form biofilms and its impact on airway epithelia using in vivo and in vitro analyses.

275 and rAAV2/5 transduction in polarized human airway epithelia using viruses purified by a newly devel

276 can restore host defences in cystic fibrosis airway epithelia via a mechanism that is independent of

277 5 (rAAV-5) is known to efficiently transduce airway epithelia via apical infection.

278 AV2/1 apical transduction of human polarized airway epithelia was 10-fold lower than that for rAAV2/2

279 Furthermore, binding and gene transfer to airway epithelia was competed by lectins that specifical

280 ria multivorans by well-differentiated human airway epithelia was investigated by immunohistology and

281 Reovirus infection of human airway epithelia was more efficient after adsorption to

282 P(Cl) /P(Na) of airway epithelia was unaltered by pH 7.4 vs.

283 tion to the apical surface of differentiated airway epithelia we found that a recombinant AAV5 bound

284 Using cultured airway epithelia, we confirmed that SPLUNC1 is criticall

285 apical gene transfer to differentiated human airway epithelia, we expressed CAR in which the transmem

286 e apically confined ER Ca(2+) stores, normal airway epithelia were chronically exposed to supernatant

287 The present study investigated whether CF airway epithelia were hyperinflammatory and, if so, whet

288 luminal mechanical stimulation in polarized airway epithelia were initiated by the release of the 5'

289 rimary cultures of well-differentiated human airway epithelia were transduced when filovirus GP-pseud

290 ghly expressed in multiple tissues including airway epithelia, where it acts as an apical conduit for

291 e-limiting step for sodium absorption across airway epithelia, which in turn regulates airway surface

292 Treating airway epithelia with an miR-138 mimic increased CFTR mR

293 rmed adherent biofilms on the apical surface airway epithelia with decreased susceptibility to antibi

294 Gene transfer to differentiated airway epithelia with existing viral vectors is very ine

295 The results indicate that airway epithelia with intact barrier function restrict i

296 monstrated that apical transduction of human airway epithelia with rAAV2/1 was 100-fold more efficien

297 the apical and basolateral membrane of human airway epithelia with similar efficiency.

298 Therefore, we generated porcine airway epithelia with varying ratios of CF and wild-type

299 vate levels of CSTA expression in lung small airway epithelia, with still further upregulation in squ

300 Infection begins in airway epithelia, with subsequent alveolar involvement a